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Sex, the Queen of Problems in Evolutionary Biology

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Sex, the Queen of Problems in Evolutionary Biology

Evolution or design? You will be amazed at the complexity and different systems needed to be in place for human reproduction to be possible! 1

http://reasonandscience.catsboard.com/t1685-sex-the-queen-of-problems-in-evolutionary-biologyy



women are born with a limited number of eggs and generally releases only one egg per cycle.
Question: without an egg release fertilisation is impossible. Therefore, would this system not have to be in place right from the beginning?
Sperms develop only 3 to 5 degrees lower than body temperature. The scrotum expands/contracts to get further/closer from the body. This keeps the sperms at the right temperature in order that they do not die.

Question: would this system not have to be fully in place right from the beginning? Otherwise, no sperms would be produced.
Sperms and eggs have each 23 chromosomes, while the other cells in humans have 46 chromosomes.

Question: how did evolution produce these highly specialized cells, which have only half of the number of chromosomes, than all the other cells ? The gender of the baby is decided by the sperm. Sperms either have x , or y chromosomes. The egg is always x.xx = girl , xy = boy. Wouldn't have both the x and the y chromosome sperm have to have been in place at the same time? Otherwise, only one gender would be produced. To have any hope of reproduction first men would have to be able to pass semen from his body to the woman's body.

Question: wouldn't this system have to be in place right from the beginning? Also, what intermediary system could there be? Either the sperm was able to leave the body, or it was not. Sperm must be able to swim. Sperm is highly specialized for the task to fertilize the egg which includes being able to swim.

Question: would sperm not need to be able to swim right from the beginning? Without being able to swim, it could not reach the egg. Sperm must find the egg. Even if they can swim, they have the huge task to find the egg. Fortunately, the egg releases progesterone as a chemoattractant that points the sperm the way to the egg.

Questions: Wouldn't this system need to be in place from the beginning? How did evolution produce sperms that can sense progesterone? And know that they have to follow it to find the egg?
Sperm has the correct enzyme on the head to be able to penetrate the egg wall. When a sperm reaches the egg it releases special enzymes which break down the tougher wall of the egg. Without these enzymes, the egg could not fertilize the egg.

Question: wouldn't this system have to be in place from the beginning? Egg outer wall hardens in order for another sperm not being able to penetrating the same egg. Fertilisation by more than one sperm inevitably leads to the death of the embryo. Shortly after the egg enters the sperm, the outer membrane hardens and becomes impenetrable to another.

Question: would this system not have to be in place right from the beginning? Sperm and egg must fuse in order their nuclei to become one. The nucleus of the egg fuses with the nucleus of the sperm uniting both genetic materials to become a new individual.

Question: How can evolution explain this? The fertilized egg must attach to the uterus wall.  The newly fertilized egg is covered in the molecule " i selectin " which enables it to stick to the uterus wall.

Question: wouldn't this molecule have to be in place right from the beginning? Without it, the egg would not attach, and the pregnancy would end. The placenta is an extremely complex piece of equipment.  it acts as the lung, kidney, and digestive system of the baby.

Question: how does evolution explain the placenta? Without it, the baby would not survive. Would it not have to be there right from the beginning with all its functions in place? Before birth, the baby gets its oxygen from the placenta. Its lungs are in a collapsed state and receive little blood supply. Most of the blood destined for the lungs is diverted through a hole between the top chambers of the heart. All of this has to change within the first moments of birth. Sensors in the baby's skin and within its blood vessels detect temperature drops and rising CO2 level which makes the baby take its first breath. The baby's lungs are coated in a fluid called surfactant which significantly reduces the force needed to inflate the lungs. The inflated lungs reduce the pressure in the heart which in turn closes the hole in the heart which in turn sends more blood to the lungs.

Questions: Wouldnt the sensors and programming to stimulate the first breath not had to have been there right from the beginning?
Conclusion: The human reproductive process is a complicated process of systems that could not have come about gradually.
Evolution, or design? definitively, design.


Human reproduction proves design not evolution

Human reproduction is made possible by an incredible system of systems. The theory of evolution proposes that things evolve gradually over time. Please bear that in mind when you read about the marvellous human reproductive system. The following is a list of the systems involved.

Asexual to sexual reproduction


The evolution from asexual to sexual is not a favorite topic of discussion in most evolutionary circles, because no matter how many theories evolutionists conjure up (and there are several), they still must surmount the enormous hurdle of explaining the origin of the first fully functional female and the first fully functional male necessary to begin the process.
Exactly how did we arrive at two separate genders (at the same time) each with its own physiology?

Female egg release system

Woman is born with a limited number of eggs and generally only releases one egg per cycle.
If this system wasn’t in place from the beginning then no eggs would be released making fertilization impossible.

Sperm development temperature

Sperm only develop in temperatures 3 – 5 degrees fahrenheit lower than the body. The scrotum has a built in thermostat. If the temperature is too cold or too hot the scrotum contracts/expands to get closer/further from the body. This keeps the sperm at the correct temperature so that they don’t die.
This system has to have been in place from the beginning or all the sperm would die?

Sperm and egg have only 23 single chromosomes

Unlike every cell of the human body, which have 46 chromosomes (in 23 pairs), these cells have only 23 (not in pairs).
How did it come to be that these cells only have 23 chromosomes?

Sperm determines whether it is a girl or a boy

The egg is always x chromosome. The sperm can be either x or y chromosome. xx = girl, xy = boy.
If sperm were only x or only y then the species would quickly die out since only one gender would be produced. Both types of sperm had to be there from the beginning?

Man being able to pass semen out of his body

Wouldn’t this system need to be in place from the start? Otherwise the sperm could not reach the egg?

Sperm must be able to swim

The sperm are highly specialized for the task of fertilizing an egg.
If sperm couldn’t swim from the beginning then they couldn’t reach the egg to fertilize it. Quite lucky that sperm can swim aren’t we?

Cervical mucus for sperm transport

The importance of normal Cervical Mucus in natural reproduction is widely recognised. For most of a woman’s cycle the Cervical Mucus is a thick gel and hostile to sperm, with a low pH and a structure that stops sperm transport by the presence of closely spaced microfibers. During ovulation, however, the Cervical Mucus becomes more alkaline (higher pH), and more fluid. This allows the sperm to swim through the mucus and into the uterus.
If this cervical mucus was not in place from the start then sperm could not reach the egg?

Semen is alkaline

The normal environment of the vagina is a hostile one for sperm, as it is very acidic and patrolled by immune cells. The seminal plasma attempts to compensate for this hostile environment.
If the seminal fluids were not alkaline then the sperm would die before reaching the egg

Sperm needs to find the egg

Cells surrounding the egg release progesterone as a “chemoattractant” that “points the sperm the way to the egg”.
The hormone also triggers a last-gasp jolt of hyperactivity in the sperm when they are close to the egg, where progesterone is highly concentrated.
“Hyperactive sperm beat their tails forcefully like a whiplash, and appear to mobilise their last reserves of strength – like marathon runners in the home stretch,”.
This final burst of energy helps the sperm penetrate the egg.How would sperm evolve to know to swim towards the female hormones?

Sperm has correct enzyme on head that can penetrate egg wall

The first sperm that reaches the egg releases a special enzyme to eat through the outer layer (zona pellucid) of the egg.
There are over 75,000 known enzymes in nature. Lucky that the sperm has the right one!

Egg outer wall hardens to prevent other sperm fertilizing the same egg

Polyspermy (more than one sperm entering the egg) is almost always fatal for the egg. To prevent this, several changes to the egg’s cell membranes renders them impenetrable shortly after the first sperm enters the egg.
Shields up! Fertilization by more than one sperm ‘polyspermy’ inevitably leads to the death of the embryo. Is it luck that this system is in place?

Sperm and egg must fuse so that their nuclei become one

The nucleus of the sperm fuses with the nucleus of the egg, uniting both genetic materials together to form a brand new individual.
What are the chances of this? It’s truly a miracle.

Fertilized egg must attach to the uterus wall

Egg is covered in a molecule called L-selectin which binds to the carbohydrates in the uterus wall!
What are the chances that the egg would be covered in the right molecule to help it attach to the uterus?

The amazing placenta

The placenta is an extremely complex piece of biological equipment. It allows the mother’s blood and the baby’s to come into very close contact – but without ever mixing. This enables blood to pass across nutrients and oxygen to the baby, and waste products like carbon dioxide to go back from baby to mother. It acts as the lung, kidney and digestive system for the baby.
The placenta continues to produce progesterone which stabilises conditions inside the uterus until birth. This is important because among other things: stimulates the growth of breast tissue, prevents lactation until after birth, strengthens the mucus plug covering the cervix to prevent infection, stops the uterus from contracting.This amazing selfless organ is vital… without it there would be no baby. It had to be there from the beginning?

Baby’s first breath

Before birth the baby is surrounded by amniotic fluid and get’s it’s oxygen from the placenta. The baby has lungs but they are in a collapsed state and receive little blood supply. Most of the blood destined for the lungs is diverted through a hole between the top chambers of the heart. All this has to change within the first few moments after birth. Sensors on the baby’s skin and within blood vessels detect temperature drops and rising carbon dioxide levels… which makes the baby takes its first breath. The lungs are coated with a special fluid called ‘surfactant’ which significantly reduces the force needed to inflate the lungs. The inflated lungs reduces the pressure in the heart which in turn closes the hole between the top two chambers which in turn sends more blood supply to the lungs!
Wouldn’t the sensors and programming to stimulate the first breath had to have been there from the beginning? Without the surfactant easing the tension in the lungs the baby would not be able to breath.. so that had to be there from the beginning too?

Mother produces milk

Amazingly, a mother’s breast milk contains everything that her baby needs including: vitamins, mineral, digestive enzymes, hormones and antibodies that help the baby fight infections. It is also only produced after childbirth and is on tap for the child when it wants it. Proponents of evolution have come up with some just so stories for the evolution of breastfeeding but no hard evidence. It is quite amazing that the mother produces food directly from her own body.


Can evolution account for this system of systems?

The human reproductive system is a highly advanced process which cannot have come about gradually. Either the sperm can follow the female hormones to the egg or they cannot. Either the sperm can penetrate the egg wall or it cannot.
If you believe that all these parts of the system can come into being at the same time by chance then you are looking at a virtually impossible odds of 1 in 2.25 sextillion and that is just with a 1 in 10 for most parts of the process!

http://nathanielclaiborne.com/the-most-uncomfortable-argument-against-common-ancestry/

The Survival Value of Half A Genital

In order for common ancestry to be true, we must all share a single common ancestor. In order for that to be true, at some point genetic reproduction would have to have evolved from being purely asexual to also including coitus (to use Sheldon Cooper’s preferred term). Keep in mind that this had to happen gradually. And not just gradually, but in two separate streams (so to speak). One set of genes in a population of organisms would need to focus on gradually perfecting the vagina, while another focuses on the penis. Somehow, this genetic adaptation needs to provide survival value to continue developing.

Supposing it does, once we have organisms with fully formed genitals, they need to find each other. And then, well, they need to get it on (or at least fumble around enough to exchange fluids). Now, there is no evidence for exactly how this took place, much less evidence that it did in fact take place. Given Coyne’s two statements in the beginning of this post, I am inclined to deny common ancestry on the basis of a comically incomplete amount of evidence. Reproduction evolving from asexual to sexual doesn’t even make sense in an evolutionary paradigm as Coyne himself points out:

Biologists still question whether any known advantage outweighs the twofold cost of sex (156).

If you see how the reasoning works you’ll understand this isn’t particularly a problem for someone already committed to evolution in its totality. Because we all share a common ancestor, at some point reproduction had to evolve into the sexual realm, and because that has clearly happened, it must offer some kind of genetic advantage even if we don’t know what it is. I don’t know about you, but that sounds like faith in the absence of evidence to me.

I can see though that if one is an evolutionist and a naturalist, there really isn’t another option. You have to believe in common ancestry because it’s part of the overall theory. Likewise, you have to believe that sexual reproduction evolved gradually even if there is no evidence that this happened because it is the only way to link lower and higher forms of life to a single spontaneous evolution of non-life to life.
The Sex Life of Fossils

What applies to the issue of common ancestry in general also applies to human-primate relations in particular. While we can find fossils of primates that no longer exist, unless we can establish reproductive connections it would be hard to both distinguish different species and put them in a proper progression.

In other words, if a species is a “reproductively isolated” population or community of organisms, how can we know who these hominid fossils were shagging? While we can determine the sex of a fossil, from I’ve read it seems like it would hard to determine the sex life of a fossil, but that’s precisely what you would need to know in order to prove it is a separate species from another similar fossil find. If they weren’t “reproductively isolated” then they might not be separate species. You may be able to establish “reproductive compatibility” (like the fact we can mate tigers and lions) but that doesn’t validate that pre-historic coitus was actually taking place.

In short, I think we would need to know quite a bit more about who these hominid fossils where shacking up with before we can really establish firm boundaries between species. We also need this kind of information to better understand the sequence of species. Until there is more clear evidence on both of these fronts, I’m inclined to deny common ancestry both in the larger sense (all of life goes back to a single organism) and in the particular sense of man’s relation to the apes. This latter sense is what unnecessarily leads scientifically naive people to rethink the creation of man in Genesis (e.g. Peter Enns’ The Evolution of Adam). If you’re able to look at the available scientific evidence with a philosopher’s eye however, this kind of revisionism is unnecessary. But who knows, one day we may have all the intimate sexual details we need to fill in the blanks.

http://www.evolutionnews.org/2011/07/spinning_fanciful_tales_about_048281.html

http://crev.info/2014/11/sex-cells/

http://www.conservapedia.com/Counterexamples_to_Evolution

For evolution to be true, every male dog, cat, horse, elephant, giraffe, fish and bird had to have coincidentally evolved with a female alongside it (over billions of years) with fully evolved compatible reproductive parts and a desire to mate, otherwise the species couldn't keep going.

http://www.geneticliteracyproject.org/2014/07/07/how-did-sex-start/

Most of the single-celled organisms in the world, like bacteria, reproduce asexually by making copies of themselves. So how did sex come to rule the animal kingdom? Scientists have been trying to figure out the origin of sex for hundreds of years, without much luck.

Asexual reproduction is more convenient and requires less effort: there’s no search for a partner and you get to pass all your genes along, from the U.K.’s National History Museum:

In many ways asexual reproduction is the better evolutionary strategy: only one parent is needed and all of their genes are passed on to the next generation.  All bacteria, most plants and even some animals reproduce asexually at least some of the time.
Sex is less efficient. Finding a mate can take time and energy, and any gametes that aren’t fertilised go to waste. Plus, each parent only passes half of its genes to the offspring.

One of the many problems with the so-called "common ancestor" fantasy is that gender-differentiation could not possibly have evolved or developed gradually, from a creature that was not gender-differentiated, as the darwinist claims. This is because reproduction of gender-differentiated offspring is an "all-or-none" scenario. Gender differentiation must necessarily have manifested 100% complete, with both genders and all of their respective organs and behaviors fully represented, or it could have never manifested at all. Such simultaneous and complete manifestation of two different genders -- along with their matching yet differentiated sexual organs as well as their matching yet differentiated sexual behaviors -- would necessarily require an immense amount of planning and organization, from an extremely powerful and extremely intelligent designer.

1. http://goddidit.org/human-reproduction/



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http://www.creationtoday.org/creationist-challenge/

http://reasonandscience.heavenforum.org/t1685-sex-the-queen-of-problems-in-evolutionary-biology

Spontaneous reproduction

What are the odds that, of the millions of species of animals, birds, fish and insects, a male of each species developed at the same time and in the same place as a female of the same species, so that the species could propagate? Why are there two sexes anyhow? This is not foreordained in the evolutionary framework. Is there some sort of plan here? If the first generation of mating species didn’t have parents, how did the mating pair get to that point? Isn’t evolution supposed to progress when an offspring of a mating pair has a beneficial mutation?

Conclusion: No parents, no evolution. A species would have to jump from a primitive form to a fully developed male and female, each with the ability and instinct to mate.



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. In his book, The Masterpiece of Nature: The Evolution of Genetics and Sexuality, Graham Bell admitted that the whole problem of sexual reproduction “represents the most important challenge to the modern theory of evolution” (1982, book jacket). He then went on to describe the dilemma in the following manner:

Sex is the queen of problems in evolutionary biology. Perhaps no other natural phenomenon has aroused so much interest; certainly none has sowed as much confusion. The insights of Darwin and Mendel, which have illuminated so many mysteries, have so far failed to shed more than a dim and wavering light on the central mystery of sexuality, emphasizing its obscurity by its very isolation (p. 19, emp. added).

The same year that Bell published his book, evolutionist Philip Kitcher noted: “Despite some ingenious suggestions by orthodox Darwinians, there is no convincing Darwinian history for the emergence of sexual reproduction” (1982, p. 54). Evolutionists since have freely admitted that the origin of gender and sexual reproduction still remains one of the most difficult problems in biology (see, for example, Maynard-Smith, 1986, p. 35). In his 2001 book, The Cooperative Gene, evolutionist Mark Ridley wrote (under the chapter title of “The Ultimate Existential Absurdity”): “Evolutionary biologists are much teased for their obsession with why sex exists. People like to ask, in an amused way, ‘isn’t it obvious?’ Joking apart, it is far from obvious…. Sex is a puzzle that has not yet been solved; no one knows why it exists”(pp. 108,111, emp. added). In an article in Bioscience on “How Did Sex Come About?,” Julie Schecter remarked:

Sir John Maddox, who served for over twentyfive years as the editor of Nature, the prestigious journal pub-lished by the British Association for the Advancement of Science (and who was knighted by Queen Elizabeth II in 1994 for his “multiple contributions to science”), authored an amazing book titled What Remains to be Discovered in which he ad-dressed the topic of the origin of sex, and stated forthrightly:Sex is ubiquitous…. Yet sex remains a mystery to researchers, to say nothing of the rest of the population. Why sex? At first blush, its disadvantages seem to outweigh its benefits. After all, a parent that reproduces sexually gives only onehalf its genes to its offspring, whereas an organism that reproduces by dividing passes on all its genes. Sex also takes much longer and requires more energy than simple division. Why did a process so blatantly unprofitable to its earliest practitioners become so widespread? (1984, 34: 680).

five years as the editor of Nature, the prestigious journal pub-lished by the British Association for the Advancement of Sci-ence (and who was knighted by Queen Elizabeth II in 1994 for his “multiple contributions to science”), authored an amaz-ing book titled What Remains to be Discovered in which he ad-dressed the topic of the origin of sex, and stated forthrightly:

The overriding question is when (and then how) sexual reproduction itself evolved. Despite decades of speculation, we do not know. The difficulty is that sexual reproduction creates complexity of the genome and the need for a separate mechanism for producing gametes. The metabolic cost of maintaining this system is huge, as is that of providing the organs specialized for sexual reproduction (the uterus of mammalian females, for example). What are the offsetting benefits? The advantages of sexual reproduction are not obvious (1998, p. 252, parenthetical items in orig., emp. added).

The fact that the advantages of sex are “not obvious” is well known (though perhaps not often discussed) within the hallowed halls of academia. J.C. Crow lamented:

Sexual reproduction seems like a lot of baggage to carry along if it is functionless. Evolutionary conservatism perpetuates relics, but does it do so on such a grand scale as this?… It is difficult to see how a process as elaborate, ubiquitous, and expensive as sexual reproduction has been maintained without serving some important purpose of its own (1988, p. 60).

What is that “purpose”? And how can evolution via natu-ral selection explain it? Would “Nature” (notice the capital “N”) “select for” sexual reproduction? As it turns out, the com-mon “survival of the fittest” mentality cannot begin to explain the high cost of first evolving, and then maintaining, the sex-ual apparatus. Sexual reproduction requires organisms to first produce, and then maintain, gametes (reproductive cells—i.e., sperm and eggs). Additionally, various kinds of incompatibil-ity factors (like the blood Rh factor between mother and child

can pass along addition-al “costs” (some of which can be life threatening) that are inherent in this “expensive” means of re-production. In sexual or-ganisms, problems also can arise in regard to tis-sue rejection between the mother and the newly formed embryo.

The human immune system

is vigilant in identifying foreign tissue (such as an embryo that carries half of the male’s genetic information), yet evolution-ists contend that the human reproductive system has “selectively evolved” this “elaborate, ubiquitous, and expensive” method of reproduction. In trying to reconcile the logic behind what causes such things to occur via naturalistic evolution, vitalist philosopher Arthur Koestler observed:

Once upon a time it all looked so simple. Nature regarded the fit with the carrot of survival and punished the unfit with the stick of extinction. The trouble only started when it came to defining “fitness.” …Thus natural selection looks after the survival and reproduction of the fittest, and the fittest are those which have the highest rate of reproduction—we are caught in a circular argument which completely begs the question of what makes evolution evolve? (1978, p. 170).

The question of “what makes evolution evolve” is especially critical when it comes to the origin of sex and sexual reproduction. As Dr. Maddox went on to say: “Much more must be learned of the course of evolution before it is known how (rather than why) sexual reproduction evolved…. That task will require intricate work by future generations of biologists” (pp. 253,254, parenthetical item in orig.). It is our contention, based on the evidence at hand, that the intricacy, complexity, and informational content associated with sexual reproduction demand the conclusion that sex is neither a “historical accident” resulting in evolutionary baggage nor a product of organic evolution itself, but rather is the product of an intelligent Creator.

FROM ASEXUAL TO SEXUAL REPRODUCTION—THE ORIGIN OF SEX

Many single-celled organisms reproduce asexually. If we all descended from these singlecelled creatures, as Margulis and Sagan have suggested, then why was the simple-yet-effi-cient method of asexual reproduction set aside in favor of sexual reproduction?

In an intriguing article titled “The Enigma of Sex and Evolution,” biologist Jerry Bergman wrote:

Evolution requires sexual reproduction to have evolved from asexual reproduction via natural selection…. The lack of evidence of any biological systems that can bridge the chasm between sexual and asexual reproduction either today or in the past is also a major difficulty with evolution theory. Actually, the complete lack of any transitional forms for all sexual traits is a huge major fossil gap. The same problem also exists here as with any transitional form: structures are useless or worse until they are at least marginally functional. This is especially true regarding reproduction, and would result in rapid extinction if the features produced by mutations were less than fully functional (1996, 33: 230, emp. in orig.).

Dobzhansky and his co-authors commented on this “enigma” in their book, Evolution:

With respect to the origin of sexual reproduction, two challenging questions present themselves. First, in what kinds of organisms did sex first arise? And sec-ond, what was the adaptive advantage that caused sexual reproduction to become predominant in higher or-ganisms? (1977, p. 391)

Asexual reproduction is the formation of new individuals from cells of only one parent, without gamete formation or fertilization by another member of the species. Asexual reproduction thus does not require one egg-producing parent and one sperm-producing parent. A single parent is all that is required. In addressing this point, evolutionist George C. Williams admitted that the “immediate advantage of asexual reproduction is generally conceded by all those who have seriously concerned themselves with the problem” (1977, p. Cool. In fact, he went on to note that

“the masculine-feminine contrast is a prima facie difficulty for evolutionary theory” (p. 124).

Sporulation (spore formation) is one method of asexual reproduction among protozoa and certain plants. A spore is a reproductive cell that produces a new organism without fertilization. In some lower forms of animals (e.g., hydra), and in yeasts, budding is a common form of asexual repro-duction as a small protuberance on the surface of the parent cell increases in size until a wall forms to separate the new in-dividual (the bud) from the parent. Regeneration is another specialized form of asexual reproduction that allows some organisms (e.g. starfish and salamanders) to replace injured or lost parts. All of these processes require only one “parent,” and work quite well in stable environments.
As they have struggled to explain the existence of sexual reproduction in nature, evolutionists have suggested four dif-ferent (and sometimes contradictory) theories, known in the literature as: (1) the Lottery Principle; (2) the Tangled Bank Hy-pothesis;(3)the Red Queen Hypothesis; and (4) theDNARe-pair Hypothesis. We would like to discuss each briefly.

In his 2001 book, Evolution: The Triumph of an Idea, Carl Zimmer admitted:

Sex is not only unnecessary, but it ought to be a recipe for evolutionary disaster. For one thing, it is an inefficient way to reproduce…. And sex carries other costs as well…. By all rights, any group of animals that evolves sexual reproduction should be promptly outcompeted by nonsexual ones. And yet sex reigns.
...Why is sex a success, despite all its disadvantages? (pp. 230,231, emp. added).


http://pages.towson.edu/scully/sex.html

"Sex is the queen of problems in evolutionary biology.
Perhaps no other natural phenomenon has aroused so much interest;
certainly none has sowed so much confusion."
- Graham Bell, 1982



http://genetics.thetech.org/original_news/news143

Solving the Sex Problem in Evolution

Sex May be More Important for Stability than Change

July 15, 2011

Explaining the evolution of sex has been a problem for a very long time. Most ideas have focused on the advantages to populations. For example, sex causes a genetic mixing which is good for a species' survival in a changing environment.

Unfortunately evolution can't work on populations - it has to have advantages for the individual as well. This is especially true for sex given its high cost to the individual (the existence of males, sexually transmitted diseases, etc.).

http://www.jstor.org/discover/10.2307/1542981?uid=4&sid=21104421048963


http://www.apologeticspress.org/apPubPage.aspx?pub=1&issue=535

http://crev.info/2014/06/sperm-cells-gain-respect/

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http://www.trueorigin.org/sex01.asp

Abstract

The origin and maintenance of sex and recombination is not easily explained by natural selection. Evolutionary biology is unable to reveal why animals would abandon asexual reproduction in favor of more costly and inefficient sexual reproduction. Exactly how did we arrive at two separate genders-each with its own physiology? If, as evolutionists have argued, there is a materialistic answer for everything, then the question should be answered: Why sex? Is sex the product of a historical accident or the product of an intelligent Creator? The current article reviews some of the current theories for why sexual reproduction exists today. Yet, as these theories valiantly attempt to explain why sex exists now, they do not explain the origin of sex. We suggest that there is no naturalistic explanation that can account for the origin and maintenance of sex.

Introduction

Biology texts illustrate amoebas evolving into intermediate organisms, which then give rise to amphibians, reptiles, mammals, and, eventually, humans. Yet, we never learn exactly when or how independent male and female sexes originated. Somewhere along this evolutionary path, both males and females were required in order to ensure the procreation that was necessary to further the existence of a particular species. But how do evolutionists explain this? When pressed to answer questions such as, “Where did males and females actually come from?,” “What is the evolutionary origin of sex?,” evolutionists become silent. How could nature evolve a female member of a species that produces eggs and is internally equipped to nourish a growing embryo, while at the same time evolving a male member that produces motile sperm cells? And, further, how is it that these gametes (eggs and sperm) conveniently “evolved” so that they each contain half the normal chromosome number of somatic (body) cells? [Somatic cells reproduce via the process of mitosis, which maintains the species’ standard chromosome number; gametes are produced via the process of meiosis, which halves that number. We will have more to say about both processes later.]

The evolution of sex (and its accompanying reproductive capability) is not a favorite topic of discussion in most evolutionary circles, because no matter how many theories evolutionists conjure up (and there are several), they still must surmount the enormous hurdle of explaining the origin of the first fully functional female and the first fully functional male necessary to begin the process. In his book, The Masterpiece of Nature: The Evolution of Genetics and Sexuality, Graham Bell described the dilemma in the following manner:

‘Sex is the queen of problems in evolutionary biology. Perhaps no other natural phenomenon has aroused so much interest; certainly none has sowed as much confusion. The insights of Darwin and Mendel, which have illuminated so many mysteries, have so far failed to shed more than a dim and wavering light on the central mystery of sexuality, emphasizing its obscurity by its very isolation.’[1]
The same year that Bell released his book, well-known evolutionist Philip Kitcher noted: “Despite some ingenious suggestions by orthodox Darwinians, there is no convincing Darwinian history for the emergence of sexual reproduction.”[2] Evolutionists since have freely admitted that the origin of gender and sexual reproduction still remains one of the most difficult problems in biology (see, for example, Maynard-Smith, 1986, p. 35). In his 2001 book, The Cooperative Gene, evolutionist Mark Ridley wrote (under the chapter title of “The Ultimate Existential Absurdity”):

‘Evolutionary biologists are much teased for their obsession with why sex exists. People like to ask, in an amused way, “isn’t it obvious?” Joking apart, it is far from obvious.... Sex is a puzzle that has not yet been solved; no one knows why it exists’[3] [emp. added].
In an article in Bioscience on “How Did Sex Come About?,” Julie Schecter remarked:

‘Sex is ubiquitous.... Yet sex remains a mystery to researchers, to say nothing of the rest of the population. Why sex? At first blush, its disadvantages seem to outweigh its benefits. After all, a parent that reproduces sexually gives only one-half its genes to its offspring, whereas an organism that reproduces by dividing passes on all its genes. Sex also takes much longer and requires more energy than simple division. Why did a process so blatantly unprofitable to its earliest practitioners become so widespread?’[4]
This “mystery” of sex deserves serious consideration in light of its “widespread” prevalence today.

“Intellectual Mischief and Confusion”
—or Intelligent Design?

Evolutionists freely admit that the origin of the sexual process remains one of the most difficult problems in biology.[5] Lynn Marguilis and Dorion Sagan have proposed a simple solution by suggesting that Mendelian inheritance and sex were a historical accident—i.e. a kind of “accidental holdover” from the era of single-celled organisms. They claim that the maintenance of sex is therefore a “nonscientific” question that “leads to intellectual mischief and confusion.”[6] This implies, however, that sex is useless, and that it has been retained through the years merely by accident. Yet even evolutionists realize the ubiquity and complexity of sexual reproduction. Niles Eldridge, a staunch evolutionist from the American Museum of Natural History, has declared: “Sex occurs in all major groups of life.”[7]

But why is this the case? Evolutionists have practically been forced to concede that there must be “some advantage” to a system as physiologically and energetically complex as sex-as Mark Ridley admitted when he wrote: “...[I]t is highly likely that sex has some advantage, and that the advantage is big. Sex would not have evolved, and been retained, unless it had some advantage”[8] (emp. added). Yet finding and explaining that advantage seems to have eluded our evolutionary colleagues. Sir John Maddox, who served for over twenty-five years as the distinguished editor of Nature, the prestigious journal published by the British Association for the Advancement of Science (and who was knighted by Queen Elizabeth II in 1994 for “multiple contributions to science”), authored an amazing book titled What Remains to be Discovered in which he addressed the topic of the origin of sex, and stated forthrightly:

‘The overriding question is when (and then how) sexual reproduction itself evolved. Despite decades of speculation, we do not know. The difficulty is that sexual reproduction creates complexity of the genome and the need for a separate mechanism for producing gametes. The metabolic cost of maintaining this system is huge, as is that of providing the organs specialized for sexual reproduction (the uterus of mammalian females, for example). What are the offsetting benefits? The advantages of sexual reproduction are not obvious’[9] [emp. added, parenthetical item in orig.].

Male Sperm Cell Attempting to Penetrate Female Egg
The fact that the advantages of sex “are not obvious” is well known (though perhaps not often discussed) within academia. J.F. Crow lamented:

‘Sexual reproduction seems like a lot of baggage to carry along if it is functionless. Evolutionary conservatism perpetuates relics, but does it do so on such a grand scale as this?... It is difficult to see how a process as elaborate, ubiquitous, and expensive as sexual reproduction has been maintained without serving some important purpose of its own.’[10]
What is that “purpose”? And how can evolution (via natural selection) explain it? As it turns out, the common “survival of the fittest” mentality cannot begin to explain the high cost of first evolving, and then maintaining, the sexual apparatus. Sexual reproduction requires organisms first to produce, and then maintain, gametes (reproductive cells-i.e., sperm and eggs).

Additionally, various kinds of incompatibility factors (such as the blood Rh factor between mother and child) pass along more “costs” (some of which can be life threatening) that are automatically inherent in this “expensive” means of reproduction. In sexual organisms, problems also can arise in regard to tissue rejection between the mother and the newly formed embryo. The human immune system is vigilant in identifying foreign tissue (such as an embryo that carries half of the male’s genetic information), yet evolutionists contend that the human reproductive system has “selectively evolved” this “elaborate, ubiquitous, and expensive” method of reproduction.

It is our contention, based on the evidence, that the intricacy, complexity, and informational content associated with sexual reproduction demand the conclusion that sex is neither a “historical accident” resulting in evolutionary baggage, nor a product of organic evolution itself, but rather is the product of an intelligent Creator.

From Asexual to Sexual Reproduction
—The Origin of Sex

Many single-celled organisms reproduce asexually. If we all descended from these single-celled creatures, as Margulis and Sagan have suggested, then why was the simple-yet-efficient method of asexual reproduction set aside in favor of sexual reproduction? Dobzhansky and his co-authors commented on this ironic difficulty in their book, Evolution:

‘With respect to the origin of sexual reproduction, two challenging questions present themselves. First, in what kinds of organisms did sex first arise? And second, what was the adaptive advantage that caused sexual reproduction to become predominant in higher organisms?’[11]

Asexual reproduction through budding.
Asexual reproduction is the formation of new individuals from cells of only one parent, without gamete formation or fertilization by another member of the species. Asexual reproduction thus does not require one egg-producing parent and one sperm-producing parent. A single parent is all that is required. Sporulation (the formation of spores) is one method of asexual reproduction among protozoa and certain plants. A spore is a reproductive cell that produces a new organism without fertilization. In certain lower forms of animals (e.g., hydra), and in yeasts, budding is a common form of asexual reproduction as a small protuberance on the surface of the parent cell increases in size until a wall forms to separate the new individual (the bud) from the parent. Regeneration is another form of asexual reproduction that allows organisms (e.g. starfish and salamanders) to replace injured or lost parts.

As they have struggled to explain the existence of sexual reproduction in nature, evolutionists have suggested four different (and sometimes contradictory) theories, known in the literature as: (1) the Lottery Principle; (2) the Tangled Bank Hypothesis; (3) the Red Queen Hypothesis; and (4) the DNA Repair Hypothesis. We would like to discuss each briefly.

The Lottery Principle

The Lottery Principle was first suggested by American biologist George C. Williams in his monograph, Sex and Evolution.[12] Williams’ idea was that sexual reproduction introduced genetic variety in order to enable genes to survive in changing or novel environments. He used the lottery analogy to get across the concept that breeding asexually would be like buying a large number of tickets for a national lottery but giving them all the same number. Sexual reproduction, on the other hand, would be like purchasing a small number of tickets, but giving each of them a different number.

The essential idea behind the Lottery Principle is that since sex introduces variability, organisms would have a better chance of producing offspring that will survive if they reproduce a range of types rather than merely more of the same. The point being made by those who advocate the Lottery Principle is that, in their view, asexual reproduction is poorly equipped to adapt to rapidly changing environmental conditions due to the fact that the offspring are exact duplicates (i.e., clones) of their parents, and thus inherently possess less genetic variation-variation that ultimately could lead to radically improved adaptability and a much greater likelihood of survival). As Carl Zimmer wrote under the title of “Evolution from Within” in his volume, Parasite Rex: “A line of clones might do well enough in a forest, but what if that forest changed over a few centuries to a prairie? Sex brought the variations that could allow organisms to survive change.”[13] Matt Ridley added:

‘...[A] sexual form of life will reproduce at only half the rate of an equivalent clonal form. The halved reproductive rate of sexual forms is probably made up for by a difference in quality: the average sexual offspring is probably twice as good as an equivalent cloned offspring’[14] [emp. added].
It would be “twice as good” or “twice as fit” of course, because it had twice the genetic endowment (having received half from each of the two parents). As Reichenbach and Anderson summarized the issue:

‘For example, why do most animals reproduce sexually rather than asexually, when asexual reproduction seems to conform best to the current theory that in natural selection the fittest are those that preserve their genes by passing them on to their progeny? One theory is that sexual reproduction provides the best defense against the rapidly reproducing, infectious species that threaten the existence of organisms. The diversity in the species that results from combining different gene pools favors the survival of those that are sexually reproduced over those that by cloning inherit repetitive genetic similarity’[15] [emp. added].
It is that “diversity in the species,” according to the principle, which helps an organism maintain its competitive edge in nature’s struggle of “survival of the fittest.” But the Lottery Principle has fallen on hard times of late. It suggests that sex would be favored by a variable environment, yet a close inspection of the global distribution of sex reveals that where environments are stable (such as in the tropics), sexual reproduction is most common. In contrast, in areas where the environment is unstable (such as at high altitudes or in small bodies or water), asexual reproduction is rife.

The Tangled Bank Hypothesis

The Tangled Bank Hypothesis suggests that sex evolved in order to prepare offspring for the complicated world around them. The “tangled bank” phraseology comes from the last paragraph of Darwin’s Origin of Species, in which he referred to a wide assortment of creatures all competing for light and food on a “tangled bank.” According to this concept, in any environment where there exists intense competition for space, food, and other resources, a premium is placed on diversification. As Zimmer described it:

‘In any environment—a tidal flat, a forest canopy, a deep-sea hydrothermal vent—the space is divided into different niches where different skills are needed for survival. A clone specialized for one niche can give birth only to offspring that can also handle the same niche. But sex shuffles the genetic deck and deals the offspring different hands. It’s basically spreading out progeny so that they’re using different resources.’[16]
The Tangled Bank Hypothesis, however, also has fallen on hard times. In his book, Evolution and Human Behavior, John Cartwright concluded:

‘Although once popular, the tangled bank hypothesis now seems to face many problems, and former adherents are falling away. The theory would predict a greater interest in sex among animals that produce lots of small offspring that compete with each other. In fact, sex is invariably associated with organisms that produce a few large offspring, whereas organisms producing small offspring frequently engage in parthenogenesis [asexual reproduction-BT/BH]. In addition, the evidence from fossils suggests that species go for vast periods of [geologic] time without changing much’[17] [emp. added].
Indeed, the evidence does suggest “that species go for vast periods of time without changing much.” Consider the following admission in light of that point. According to Margulis and Sagan, bacteria “evolved” in such a fashion as to ultimately be responsible for sexual reproduction. Yet if that is the case, why, then, have the bacteria themselves remained virtually unchanged—from an evolutionary viewpoint—for billions of years of Earth history? In his book, Evolution of Living Organisms, the eminent French zoologist, Pierre-Paul Grassé, raised this very point.

‘[B]acteria, despite their great production of intraspecific varieties, exhibit a great fidelity to their species. The bacillus Escherichia coli, whose mutants have been studied very carefully, is the best example. The reader will agree that it is surprising, to say the least, to want to prove evolution and to discover its mechanisms and then to choose as a material for this study a being which practically stabilized a billion years ago’[18] [emp. added].
Additionally, it should be noted that today we still see organisms that reproduce asexually, as well as organisms that reproduce sexually—which raises the obvious question: Why do some organisms continue to reproduce asexually, while others have “evolved” the ability to reproduce sexually? Don’t the asexual organisms ever “need” genetic variety in order to enable genes to survive in changing or novel environments (the Lottery Principle)? Don’t they ever “need” to prepare their offspring for the complicated world around them (the Tangled Bank Hypothesis)?

The Red Queen Hypothesis

The Red Queen Hypothesis was first suggested by Leigh Van Valen in an article titled “A New Evolutionary Law” in Evolutionary Theory.[19] His research suggested that the probability of organisms becoming extinct bears no relationship to how long they already may have survived. In other words, as Cartwright put it: “It is a sobering thought that the struggle for existence never gets any easier; however well adapted an animal may become, it still has the same chance of extinction as a newly formed species.”[20] Biologists came to refer to the concept as the Red Queen Hypothesis, named after the character in Lewis Carroll’s Through the Looking Glass who took Alice on a lengthy run that actually went nowhere. As the queen said to poor Alice, “Now, here, you see, it takes all the running you can do, to keep in the same place.” Think of it as a “genetics arms race” in which an animal constantly must run the genetic gauntlet of being able to chase its prey, elude predators, and resist infection from disease-causing organisms. In the world of the Red Queen, organisms have to run fast-just to stay still! That is to say, they constantly have to “run to try to improve” (and the development of sex would be one way of accomplishing that). Yet doing so provides no automatic guarantee of winning the struggle known as “survival of the fittest.” “Nature,” said the eminent British poet Lord Tennyson, is “red in tooth and claw.” Currently, the Red Queen Hypothesis seems to be the favorite of evolutionists worldwide in attempting to explain the reason as to the “why” of sex.

The DNA Repair Hypothesis

Think about this. Why are babies born young? Stupid question—with a self-evident answer, right? Evolutionists suggest otherwise. The point of the question is this. Our somatic (body) cells age. Yet cells of a newborn have had their clocks “set back.” Somatic cells die, but the germ line seems to be practically immortal. Why is this the case? How can “old” people produce “young” babies? In a landmark article published in 1989, Bernstein, Hopf, and Michod suggested that they had discovered the answer:

‘We argue that the lack of ageing of the germ line results mainly from repair of the genetic material by meiotic recombination during the formation of germ cells. Thus our basic hypothesis is that the primary function of sex is to repair the genetic material of the germ line.’[21]
DNA can be damaged in at least two ways. First, ionizing radiation or mutagenic chemicals can alter the genetic code. Or, second, a mutation can occur via errors during the replication process itself. Most mutations are deleterious (see Cartwright[22]). In an asexual organism, by definition, any mutation that occurs in one generation will be passed on automatically to the next. In his book, The Red Queen,[23] Matt Ridley compared it to what occurs when you photocopy a document, then photocopy the photocopy, and then photocopy that photocopy, etc. Eventually, the quality deteriorates severely. Asexual organisms, as they continue to accumulate mutations, face the unpleasant prospect of eventually becoming both unable to reproduce and unviable-neither of which would be at all helpful to evolution. [Commonly known as Muller’s Ratchet hypothesis, the mechanism operates like a downward ratchet on asexual populations with any deleterious mutation that occurs in a vertically transmitted organism.]

But sexual reproduction allows most plants and animals to create offspring with good copies of two genes via crossover and would thus, help eliminate this downward ratchet since mutations, although they might still be passed on from one generation to the next, would not necessarily be expressed in the next generation (a mutation must appear in the genes of both parents before it is expressed in the offspring). As Cartwright put it:

‘In sexually reproducing species on the other hand, some individuals will be “unlucky” and have a greater share than average of deleterious mutations in their genome, and some will be “lucky,” with a smaller share. The unlucky ones will be selected out. This in the long term has the effect of constantly weeding out harmful mutations through the death of those that bear them.... Deleterious mutations...would have devastating consequences if it were not for sexual reproduction.’[24]
But, as Cartwright went on to admit: “This theory is not without its problems and critics.”[25] One of those problems, expressed by Mark Ridley (no kin to Matt), is: “We do not know for sure that sex exists to purge bad genes.”[26] No, we certainly do not! And, in fact, evidence is beginning to mount that perhaps the DNA Repair Hypothesis is itself in need of “repair.” As Maddox noted:

‘One view is that sexual reproduction makes it easier for an evolving organism to get rid of deleterious changes. That should certainly be the case if there is more than one genetic change and if their combined effect on the fitness of the evolving organisms is greater than the sum of their individual changes acting separately. But there is no direct evidence to show that this rule is generally applicable’[27] [emp. added].
We must not overlook an important fact throughout all of this: These theories valiantly attempt to explain why sex exists now, but they do not explain the origin of sex. How, exactly, did nature accomplish the “invention” of the marvelous process we know as sex? In addressing this very issue, Maddox asked quizzically:

‘How did this process (and its complexities) evolve?... The dilemma is that natural selection cannot anticipate changes in the environment, and so arrange for the development of specialized sexual organs as a safeguard against environmental change’[28] [emp. added, parenthetical item in orig.].
Exactly our point! It is one thing to develop a theory or hypothesis to explain something that already exists, but it is entirely another to develop a theory or hypothesis to explain why that something (in this case, sex) does exist. As Mark Ridley begrudgingly admitted: “Sex is not used simply for want of an alternative. Nothing, in an evolutionary sense, forces organisms to reproduce sexually”[29] [emp. added].

Perhaps Cartwright summarized the issue well when he said: “There is perhaps no single explanation for the maintenance of sex in the face of severe cost.”[30] Since he is speaking of a strictly naturalistic explanation, we would agree wholeheartedly. But we would suggest that there is no naturalistic explanation at all for the origin or maintenance of sex.

WHY SEX?

Why, then, does sex exist? In his 2001 book, Evolution: The Triumph of an Idea, Carl Zimmer admitted:

‘Sex is not only unnecessary, but it ought to be a recipe for evolutionary disaster. For one thing, it is an inefficient way to reproduce.... And sex carries other costs as well.... By all rights, any group of animals that evolves sexual reproduction should be promptly outcompeted by nonsexual ones. And yet sex reigns... Why is sex a success, despite all its disadvantages?’[31] [emp. added].
From an evolutionary viewpoint, sex definitely is “an inefficient way to reproduce.” Think about all the sexual process entails, including the complexity involved in reproducing the information carried within the DNA. It is the complexity of this process, and the manner in which it is copied from generation to generation, which practically drove Mark Ridley to distraction in The Cooperative Gene.

‘No one in human culture would try the trick of first making two copies of a message, then breaking each into short bits at random, combining equal amounts from the two to form the version to be transmitted, and throwing the unused half away. You only have to think of sex to see how absurd it is. The “sexual” method of reading a book would be to buy two copies, rip the pages out, and make a new copy by combining half the pages from one and half from the other, tossing a coin at each page to decide which original to take the page from and which to throw away’[32] [emp. added].
Again, from an evolutionary viewpoint, sex would be considered “absurd.” But from a design viewpoint, it is nothing short of incredible!

Yet there is an even more important question than why sex exists. How did sex come to exist? Evolution is dependent on change (the English word “evolution” derives from the Latin evolvere, meaning “to unroll, to change”). Quite obviously, if everything remained the same, there would be no evolution. Evolutionists believe that the driving forces behind evolution are natural selection and genetic mutations occurring over lengthy spans of geologic time (see Peter Ward[33]). Mutations are primarily the result of mistakes that occur during DNA replication. There are three different types of mutations: beneficial, deleterious, and neutral (see Mayr[34]). Neutral mutations (which admittedly do occur) are, as their name implies, “neutral.” They do not “propel” evolution forward in any significant fashion. Deleterious mutations “will be selected against and will be eliminated in due time.”[35] That, then, leaves beneficial mutations, which, according to evolutionists, are incorporated into the species by natural selection, eventually resulting in new and different organisms.

But what does all of this have to do with the origin of sex? Evolutionists adhere to the view that the first organisms on Earth were asexual, and thus they believe that, during billions of years of Earth history, asexual organisms experienced numerous beneficial mutations that caused them to evolve into sexual organisms. But the change of a single-celled, asexual prokaryote (like a bacterium) into a multi-celled, sexual eukaryote would not be a “magical” process carried out by just a few, well-chosen beneficial mutations (as if nature had the power to “choose” anything!). In fact, quite the opposite would be true. Why so? Ernst Mayr, who undeniably ranks as the most eminent evolutionary taxonomist in the world, remarked in his book, What Evolution Is: “Any mutation that induces changes in the phenotype [the outward, physical make-up of an organism-BT/BH] will either be favored or discriminated against by natural selection.... [T]he occurrence of new beneficial mutations is rather rare”[36] [emp. added]. Beneficial mutations (viz., those that provide additional information for, and instructions to, the organism) are indeed “rather rare.” Furthermore, as evolutionists have been known to admit quite candidly, mutations that affect the phenotype almost always are harmful (see Crow[37]; Cartwright[38]). The famous Stanford University geneticist, Luigi Cavalli-Sforza (who is the head of the International Human Genome Project), addressed this fact when he wrote:

‘Evolution also results from the accumulation of new information. In the case of a biological mutation, new information is provided by an error of genetic transmission (i.e., a change in the DNA during its transmission from parent to child). Genetic mutations are spontaneous, chance changes, which are rarely beneficial, and more often have no effect, or a deleterious one’[39] [emp. added, parenthetical item in orig.].
In addressing the complete ineffectiveness of mutations as an alleged evolutionary mechanism, Dr. Grassé observed:

‘No matter how numerous they may be, mutations do not produce any kind of evolution.... The opportune appearance of mutations permitting animals and plants to meet their needs seems hard to believe. Yet the Darwinian theory is even more demanding: a single plant, a single animal would require thousands and thousands of lucky, appropriate events. Thus, miracles would become the rule: events with an infinitesimal probability could not fail to occur.... There is no law against daydreaming, but science must not indulge in it’[40] [emp. added].
Grassé is not the only prominent evolutionist to take such a view in regard to mutations as an ineffectual driving force for evolution. In a speech presented at Hobart College several years ago, the late Harvard paleontologist Stephen Jay Gould spoke out in a somewhat militant fashion about the subject when he said:

‘A mutation doesn’t produce major new raw material. You don’t make a new species by mutating the species.... That’s a common idea people have; that evolution is due to random mutations. A mutation is not the cause of evolutionary change.’[41]
All of this raises the question: If mutations are not the cause of evolutionary change, then what is?


There is more to the problem of the origin of sex, however, than “just” the fact of rare, beneficial mutations and their much-more-frequent cousins, the harmful, deleterious mutations. There is the added problem related to the two different types of cell division we mentioned earlier-mitosis and meiosis. During mitosis, all of the chromosomes are copied and passed on from the parent cell to the daughter cells. Meiosis (from the Greek meaning to split), on the other hand, occurs only in sex cells (i.e., eggs and sperm); during this type of replication, only half of the chromosomal material is copied and passed on. [For an excellent, up-to-date description of the complicated, two-part process by which meiosis occurs, see Mayr[42]] Once meiosis has taken place,

‘[t]he result is the production of completely new combinations of the parental genes, all of them uniquely different genotypes [the genetic identity of an individual that does not show as outward characteristics-BT/BH]. These, in turn, produce unique phenotypes, providing unlimited new material for the process of natural selection’[43] [emp. added].
It is those very facts—that meiosis allegedly has “evolved” the ability to halve the chromosome number (but only for gametes), and that it actually can provide “unlimited new material”—which make the meiotic process so incredible. And the critical nature of meiosis to life as we know it has been acknowledged (albeit perhaps begrudgingly) even by evolutionists. Margulis and Sagan, for example, wrote:

‘We think that meiosis became tied to two-parent sex and that meiosis as a cell process, rather than two-parent sex, was a prerequisite for evolution of many aspects of animals.... [M]eiosis seems intimately connected with complex cell and tissue differentiation. After all, animals and plants return every generation to a single nucleated cell’[44] [emp. added].
These two evolutionists have admitted that meiosis is critical for sexual reproduction. Yet in their volume, Slanted Truths, they stated unequivocally that meiotic sex evolved “520 million years ago.”[45] How, pray tell, could the bacteria that are supposed to be responsible for the evolution of sex have “stabilized a billion years ago” (as Grassé observed that they did), and then 500 million years after that stabilization, mutate enough to “evolve” the painstaking process of meiosis? At some point authors must be questioned as to the rationale in their thinking? Read carefully the following scenario, as set forth in Jennifer Ackerman’s 2001 book, Chance in the House of Fate, and as you do, concentrate on the items we have placed in bold print that are intended to draw the reader’s attention to the “just-so” nature of the account being proffered.

‘The first sex cells may have been interchangeable and of roughly the same size. By chance, some may have been slightly bigger than others and stuffed with nutrients, an advantage in getting progeny off to a good start. Perhaps some were smaller, faster, good at finding mates. As organisms continued to meld and join their genetic material, the pairs of a larger cell with a smaller one proved an efficient system. Over time, the little rift between the sexes widened, as did the strategies of male and female for propagating their own genes’[46] [emp. added].
The first sex cells may have been.... By chance, some may have been.... Perhaps some were.... Over time, the.... It is little wonder that, in their more candid moments, evolutionists admit, as Ackerman eventually did, that “when it comes to sex, we inhabit a mystery.”[47]

Notice, however, the admission by Margulis and Sagan that “meiosis seems connected with complex cell and tissue differentiation.” Indeed it does—now! But how did a process as incredibly complex as meiosis ever get started in the first place? What (or, better yet, Who) “intricately connected it with complex cell and tissue differentiation”? With all due respect, there is not an evolutionist on the planet who has been able to come up with an adequate (much less believable) explanation as to how somatic cells reproduce by mitosis (thereby maintaining the species’ standard chromosome number in each cell), while gametes are produced by meiosis—wherein that chromosome number is halved so that, at the union of the male and female gametes during reproduction, the standard number is reinstated.

Conclusion

Lewis Thomas, the highly regarded medical doctor who served for many years as the president and chancellor of the prestigious Sloan-Kettering Cancer Center in Manhattan, was unable to contain either his enthusiasm or his praise for the system we know as “sexual reproduction.” In his book, The Medusa and the Snail, he wrote about the “miracle” of how one sperm cell forms with one egg cell to produce the cell we know as a zygote, which, nine months later, will become a newborn human being. He concluded:

‘The mere existence of that cell should be one of the greatest astonishments of the earth. People ought to be walking around all day, all through their waking hours, calling to each other in endless wonderment, talking of nothing except that cell.... If anyone does succeed in explaining it, within my lifetime, I will charter a skywriting airplane, maybe a whole fleet of them, and send them aloft to write one great exclamation point after another around the whole sky, until all my money runs out.’[48]
Dr. Thomas’ money is perfectly safe. No one has been able to explain—from an evolutionary viewpoint—the origin of sex, the origin of the incredibly complex meiotic process that makes sex possible, or the intricate development of the embryo (which is itself a marvel of design). At conception, the chromosomes inherited from the sperm are paired with the chromosomes inherited from the egg to give the new organism its full chromosomal complement. Evolutionary theorists ask us to believe that random, chance occurrences brought about this marvelously interdependent process of, first, splitting the genetic information into equal halves, and, second, recombining it through sexual reproduction. Not only is an intricate process required to produce a sperm or egg cell in the first place via meiosis, but another equally intricate mechanism also is required to rejoin the genetic information during fertilization in order to produce the zygote, which will become the embryo, which will become the fetus, which eventually will become the newborn. The idea that all of this “just evolved” is unworthy of consideration or acceptance, especially in light of the evidence now at hand.

The highly complex and intricate manner in which the human body reproduces offspring is not a matter of mere chance or a “lucky role of the dice.” Rather, it is the product of an intelligent Creator. Albert Einstein said it well when he stated: “God does not play dice with the universe.”[49]

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General Introduction: My long-term goal is to understand the evolution of sexual reproduction. For many non-biologists the biggest barrier to understanding this field is accepting that , for biologists, sex poses a serious problem .

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6 Fertilization on Fri Dec 21, 2018 3:34 am

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Fertilization

Fertilization is the process where by THE GAMETES—sperm and egg—fuse together to begin the creation of a new organism. Fertilization accomplishes two separate ends: sex (the combining of genes derived from two parents) and reproduction (the generation of a new organism). Thus, the first function of fertilization is to transmit genes from parent to offspring, and the second is to initiate in the egg cytoplasm those reactions that permit development to proceed. Although the details of fertilization vary from species to species, it generally consists of four major events:

1. Contact and recognition between sperm and egg. In most cases, this ensures that the sperm and egg are of the same species.
2. Regulation of sperm entry into the egg. Only one sperm nucleus can ultimately unite with the egg nucleus. This is usually accomplished by allowing only one sperm to enter the egg and actively inhibiting any others from entering.
3. Fusion of the genetic material of sperm and egg.
4. Activation of egg metabolism to start development.

During fertilization, the egg and sperm must meet, the genetic material of the sperm must enter the egg, and the fertilized egg must initiate cell division and the other processes of development. Sperm and egg must travel toward each other, and chemicals from the eggs can attract the sperm. Gamete recognition occurs when proteins on the sperm cell membrane meet proteins on the extracellular coating of the egg. In preparation for this meeting, the sperm cell membrane is altered significantly by exocytotic events. The sperm activates development by releasing calcium ions (Ca2+) from within the egg. These ions stimulate the enzymes needed for DNA synthesis, RNA synthesis, protein synthesis, and cell division. The sperm and egg pronuclei travel toward one another and the genetic material of the gametes combines to form the diploid chromosome content carrying the genetic information for the development of a new organism.

Sperm anatomy 
Each sperm cell consists of a haploid nucleus, a propulsion system to move the nucleus, and a sac of enzymes that enable the nucleus to enter the egg. In most species, almost all of the cell’s cytoplasm is eliminated during sperm maturation, leaving only certain organelles that are modified for spermatic function (Figure A,B below). During the course of maturation, the sperm’s haploid nucleus becomes very streamlined and its DNA becomes tightly compressed. In front or to the side of this compressed haploid nucleus lies the acrosomal vesicle, or acrosome (Figure C). The acrosome is derived from the cell’s Golgi apparatus and contains enzymes that digest proteins and complex sugars. Enzymes stored in the acrosome create a path through the outer coverings of the egg. In many species, a region of globular actin proteins lies between the sperm nucleus and the acrosomal vesicle. These proteins are used to extend a fingerlike acrosomal process from the sperm during the early stages of fertilization. In sea urchins and numerous other species, recognition between sperm and egg involves molecules on the acrosomal process. Together, the acrosome and nucleus constitute the sperm head. The means by which sperm are propelled vary according to how the species is adapted to environmental conditions. In most species, an individual sperm is able to travel by whipping its flagellum. The major motor portion of the flagellum is the axoneme, a structure formed by microtubules emanating from the centriole at the base of the sperm nucleus. The core of the axoneme consists of two central microtubules surrounded by a row of nine doublet microtubules. These microtubules are made exclusively of the dimeric protein tubulin. Although tubulin is the basis for the structure of the flagellum, other proteins are also critical for flagellar function. The force for sperm propulsion is provided by dynein, a protein attached to the microtubules. Dynein is an ATPase—an enzyme that hydrolyzes ATP, converting the released chemical energy into mechanical energy that propels the sperm. This energy allows the active sliding of the outer doublet microtubules, causing the flagellum to bend. The ATP needed to move the flagellum and propel the sperm comes from rings of mitochondria located in the midpiece of the sperm (see Figure B). In many species (notably mammals), a layer of dense fibers has interposed itself between the mitochondrial sheath and the cell membrane. This fiber layer stiffens the sperm tail. Because the thickness of this layer decreases toward the tip, the fibers probably prevent the sperm head from being whipped around too suddenly. Thus, the sperm cell has undergone extensive modification for the transport of its nucleus to the egg. In mammals, the differentiation of sperm is not completed in the testes. Although they are able to move, the sperm released during ejaculation do not yet have the capacity to bind to and fertilize an egg. The final stages of sperm maturation, cumulatively referred to as capacitation, do not occur in mammals until the sperm has been inside the female reproductive tract for a certain period of time.




The egg
cytoplasm and nucleus. 
All the material necessary to begin growth and development must be stored in the egg, or ovum. Whereas the sperm eliminates most of its cytoplasm as it matures, the developing egg (called the oocyte before it reaches the stage of meiosis at which it is fertilized) not only conserves the material it has, but actively accumulates more. The meiotic divisions that form the oocyte conserve its cytoplasm rather than giving half of it away; at the same time, the oocyte either synthesizes or absorbs proteins such as yolk that act as food reservoirs for the developing embryo. Birds’ eggs are enormous single cells, swollen with accumulated yolk. Even eggs with relatively sparse yolk are large compared to sperm. The volume of a sea urchin egg is more than 10,000 times the volume of sea urchin sperm. So even though sperm and egg have equal haploid nuclear components, the egg accumulates a remarkable cytoplasmic storehouse during its maturation. 


Discoidal meroblastic cleavage in a chick egg. 
(A) Avian eggs include some of the largest cells known (inches across), but cleavage takes place in only a small region. The yolk fills up the entire cytoplasm of the egg cell, with the exception of a small blastodisc in which
cleavage and development will take place. The chalaza are protein strings that keep the yolky egg cell centered in the shell. The albumin (egg white) is secreted onto the egg in its passage out of the oviduct. 
(B) Early cleavage stages viewed from the animal pole (the future dorsal side of the embryo). In the micrographs, the tightly apposed cell membranes have been stained with phalloidin (green). 
(C) Schematic view of cellularization in the chick egg during the day it is fertilized and still inside the hen. The numbers refer to the layers of cells.

This cytoplasmic trove includes the following:

Nutritive proteins. The early embryonic cells must have a supply of energy and amino acids. In many species, this is accomplished by accumulating yolk proteins in the egg. Many of these yolk proteins are made in other organs
(e.g., liver, fat bodies) and travel through the maternal blood to the oocyte.
Ribosomes and tRNA. The early embryo must make many of its own structural proteins and enzymes, and in some species there is a burst of protein synthesis soon after fertilization. Protein synthesis is accomplished by ribosomes and tRNA that exist in the egg. The developing egg has special mechanisms for synthesizing ribosomes; certain amphibian oocytes produce as many as 10^12 ribosomes during their meiotic prophase.
Messenger RNAs. The oocyte not only accumulates proteins, it also accumulates mRNAs that encode proteins for the early stages of development. It is estimated that sea urchin eggs contain thousands of different types of mRNA
that remain repressed until after fertilization.
Morphogenetic factors. Molecules that direct the differentiation of cells into certain cell types are present in the egg. These include transcription factors and paracrine factors. In many species, they are localized in different regions of the egg and become segregated into different cells during cleavage.
Protective chemicals. The embryo cannot run away from predators or move to a safer environment, so it must be equipped to deal with threats. Many eggs contain ultraviolet filters and DNA repair enzymes that protect them from sunlight, and some eggs contain molecules that potential predators find distasteful. The yolk of bird eggs contains antibodies that protect the embryo against microbes.

Within the enormous volume of egg cytoplasm resides a large nucleus. In a few species (such as sea urchins), this female pronucleus is already haploid at the time of fertilization. In other species (including many worms and most mammals), the egg nucleus is still diploid—the sperm enters before the egg’s meiotic divisions are completed. 


Stages of egg maturation at the time of sperm entry in different animal species. 
Note that in most species, sperm entry occurs before the egg nucleus has completed meiosis. The germinal vesicle is the name given to the large diploid nucleus of the primary oocyte. The polar bodies are nonfunctional cells
produced by meiosis

In these species, the final stages of egg meiosis will take place after the sperm’s nuclear material—the male pronucleus—is already inside the egg cytoplasm. 

Cell membrane and extracellular envelope 
The membrane enclosing the egg cytoplasm regulates the flow of specific ions during fertilization and must be capable of fusing with the sperm cell membrane. Outside this egg cell membrane is an extracellular matrix that forms a fibrous mat around the egg and is often involved in sperm-egg recognition. In invertebrates, this structure is usually called the vitelline envelope (Figure A).


Sea urchin egg cell surfaces
(A) Scanning electron micrograph of an egg before fertilization. The cell membrane is exposed where the vitelline envelope has been torn. 
(B) Transmission electron micrograph of an unfertilized egg, showing microvilli and cell membrane, which are closely covered by the vitelline envelope. A cortical granule lies directly beneath the cell membrane.

The vitelline envelope contains several different glycoproteins. It is supplemented by extensions of membrane glycoproteins from the cell membrane and by proteinaceous “posts” that adhere the vitelline envelope to the cell membrane. The vitelline envelope is essential for the species-specific binding of sperm. Many types of eggs also have a layer of egg jelly outside the vitelline envelope. This glycoprotein meshwork can have numerous
functions, but most commonly it is used either to attract or to activate sperm. The egg, then, is a cell specialized for receiving sperm and initiating development. Lying immediately beneath the cell membrane of most eggs is a thin layer (about 5 μm) of gel-like cytoplasm called the cortex. The cytoplasm in this region is stiffer than the internal cytoplasm and contains high concentrations of globular actin molecules. During fertilization, these actin molecules polymerize to form long cables of actin microfilaments. Microfilaments are necessary for cell division. They are also used to extend the egg surface into small projections called microvilli, which may aid sperm entry into the cell (Fig ure B above). Also within the cortex are the cortical granules (see B). These membrane-bound, Golgi-derived structures contain proteolytic enzymes and are thus homologous to the acrosomal vesicle of the sperm. However,
whereas a sea urchin sperm contains just one acrosomal vesicle, each sea urchin egg contains approximately 15,000 cortical granules. In addition to digestive enzymes, the cortical granules contain mucopolysaccharides, adhesive glycoproteins, and hyalin protein. As we will soon describe, the enzymes and mucopolysaccharides help prevent polyspermy—that is, they prevent additional sperm from entering the egg after the first sperm has entered—while hyalin and the adhesive glycoproteins surround the early embryo, providing support for cleavage-stage blastomeres. In mammalian eggs, the extracellular envelope is a separate, thick matrix called the zona pellucida. The mammalian egg is also surrounded by a layer of cells called the cumulus.

Spermiogenesis: the differentiation of the sperm
The production of mature and motile sperm is a detailed process that utilizes many molecular players to ensure the faithful execution of spermatogenesis. Spermatogenesis begins with a single cell that undergoes dramatic transformation, culminating with the hypercompaction of DNA into the sperm head by replacing histones with protamines. Precise execution of the stages of spermatogenesis results in the production of motile sperm. Spermatogenesis is a highly orchestrated process that requires the correct interplay and timing of all molecular constituents to produce fully functional and motile sperm. Defects in spermatogenesis can impact a male’s overall fitness, which encompasses the ability to both survive and reproduce successfully. Aberrations during any stage within spermatogenesis can have profound effects on sperm quantity, motility, morphology and ability to fertilize an egg. In addition, poor packaging of chromatin within sperm nuclei can reduce the protection of DNA against chemical and physical damage, potentially leading to mutations and unfit offspring. Modifications to sperm chromatin require the use of specialized DNA-binding proteins, referred to as protamines, which are capable of achieving the level of organization and compression necessary to fit the haploid genome into the compact sperm head.

Sperm were discovered in the 1670s, but their role in fertilization was not discovered until the mid-1800s. It was only in the 1840s, after Albert von Kölliker described the formation of sperm from cells in the adult testes that fertilization research could really begin. Even so, von Kölliker denied that there was any physical contact between sperm and egg. He believed that the sperm excited the egg to develop in much the same way a magnet communicates its presence to iron. The first description of fertilization was published in 1847 by Karl Ernst von Baer, who showed the union of sperm and egg in sea urchins and tunicates. He described the fertilization envelope, the migration of the sperm nucleus to the center of the egg, and the subsequent early cell divisions of development. In the 1870s, Oscar Hertwig and Herman Fol repeated this work and detailed the union of the two cells’ nuclei.

A complex dialogue exists between egg and sperm. The egg activates the sperm metabolism that is essential for fertilization, and the sperm reciprocates by activating the egg metabolism needed for the onset of development.

In male humans, the process of spermatogenesis supports a production rate of approximately 120 million mature spermatozoa per day by the human testis (approximately 1000 per heartbeat!). Spermatogenesis, the process by
which stem cells (spermatogonia) differentiate into mature spermatozoa, proceeds in three functionally distinct phases:
(1) the mitotic or proliferative phase, during which the majority of spermatogonia undergo mitosis to renew the stem cell pool and a minority become committed to further differentiation to produce spermatocytes; 
(2) the meiotic phase, during which spermatocytes undergo successive meiotic divisions to produce haploid germ cells (spermatids); and 
(3) spermiogenesis, during which immature, round spermatids differentiate into mature spermatozoa


Schematic diagram of human spermatogenesis. 
Spermatogonial stem cells undergo self-renewal by mitotic division. At the initiation of spermatogenesis, some spermatogonia undergo differentiation into primary spermatocytes, which contain a diploid number of chromosomes (2N = 46 chromosomes). The primary spermatocytes then undergo two successive meiotic divisions to form spermatids, which contain a haploid number of chromosomes (1N = 23 chromosomes). Spermatids undergo spermiogenesis to form mature spermatozoa, which also contain a haploid number of chromosomes. 

The mammalian haploid a spermatid is a round, unflagellated cell that looks nothing like the mature vertebrate sperm. The next step in sperm maturation, then, is spermiogenesis, the differentiation of the sperm cell. For fertilization to occur, the sperm has to meet and bind with an egg, and spermiogenesis prepares the sperm for these functions of motility and interaction. In many organisms (e.g., humans, mice, Drosophila), male germ cells undergo a series of morphological transformations during spermiogenesis to build a sperm with its typical species-specific shape from an initially round cell


Modification of a germ cell to form a mammalian sperm. 
(A) The centriole produces a long flagellum at what will be the posterior end of the sperm. The Golgi apparatus forms the acrosomal vesicle at the future anterior end. Mitochondria collect around the flagellum near the base of the haploid nucleus and become incorporated into the midpiece (“neck”) of the sperm. The remaining cytoplasm is jettisoned, and the nucleus condenses. The size of the mature sperm has been enlarged relative to the other stages. 
(B) Mature bull sperm. The DNA is stained blue, mitochondria are stained green, and the tubulin of the flagellum is stained red. 
(C) The acrosomal vesicle of this mouse sperm is stained green by the fusion of proacrosin with green fluorescent protein (GFP).


The eight steps of spermatid differentiation during spermiogenesis
A: acrosome, 
An: annulus, 
Ax: axoneme, 
C: centriole, 
F: flowerlike structures, 
Fs: flagellar substructures, 
M: mitochondria, 
Mp: middle piece, 
Mt: manchette microtubules, 
N: nucleus, 
Ne: neck (connecting piece), 
PP: principal piece, 
R: ribs of the fibrous sheath, 
Sb: spindle-shaped body. 


The acrosome of STEP 1 spermatids is oriented toward the seminiferous tubule lumen. When progressing to step 2, spermatids rotate 180° so that the acrosome faces the seminiferous tubule basement membrane.

The first step is the construction of the acrosomal vesicle b from the Golgi apparatus, a process about which we know very little. The acrosome forms a cap that covers the sperm nucleus. As the acrosomal cap is formed, the nucleus rotates so that the cap faces the basal lamina of the seminiferous tubule c . This rotation is necessary because the flagellum, which is beginning to form from the centriole on the other side of the nucleus, will extend into the lumen of the seminiferous tubule. During the last stage of spermiogenesis, the nucleus flattens and condenses, the remaining cytoplasm (the residual body, or cytoplasmic droplet) is jettisoned, and the mitochondria form a ring around the base of the flagellum.

During spermiogenesis, the histones of the spermatogonia are often replaced by sperm-specific histone variants, and widespread nucleosome dissociation takes place. This remodelling of nucleosomes might also be the point at which the Primordial germ cells (PGC) pattern of methylation is removed and the male genome-specific pattern of methylation is established on the sperm DNA. As spermiogenesis ends, the histones of the haploid nucleus are eventually replaced by protamines. This replacement results in the complete shutdown of transcription in the nucleus and facilitates the nucleus assuming an almost crystalline structure. The resulting sperm then enter the lumen of the seminiferous tubule. Unexpectedly, the sperm continue to develop after they leave the testes. When being transported from the testes, sperm reside in the epididymis. During this residence, the epididymal cells release exosomes that fuse with the sperm. These exosomes have been shown to contain small ncRNAs and other factors that can activate and repress certain genes, and the sperm will bring these agents into the egg. And the sperm still isn’t fully mature, even when it exits the urethra. The final differentiation of the sperm occurs in the reproductive tract of the female. Here, secretions from the oviducts will change the sperm cell membrane so that it can fuse with the membrane of the egg cell. Thus, the full differentiation of the sperm take place in two different organisms.

Each day, some 100 million sperm are made in each human testicle, and each ejaculation releases 200 million sperm. Unused sperm are either resorbed or passed out of the body in urine. During his lifetime, a human male can produce 10^12 to 10^13 sperm.

Spermatozoa arise within testicular seminiferous tubules by spermatogenesis, the series of cell processes by which undifferentiated germ cells give rise to mature spermatozoa. It comprises three sequential phases:

1) Mitotic multiplication/differentiation of spermatogonia, resulting in a geometric numerical expansion, loss of their stem cell properties and further commitment to advance in spermatogenesis. This phase yields a large
number of spermatogonia ready to undergo meiotic division.
(2) Meiosis, a series of two coupled cell divisions leading to genomic recombination and haploidization. These processes occur during the prophase of Meiosis I by pairing and genetic recombination between homologous
chromosomes and are followed by reduction of chromosomal numbers. Each resulting secondary spermatocyte, a unique combination of the male paternal and maternal genomes, goes into Meiosis II and generates two haploid spermatids ready to go through the last phase of spermatogenesis.
(3) Spermiogenesis, through which newly formed postmeiotic round spermatids undergo a complex cell differentiation leading to the production of elongated spermatids that leave the germinal epithelium to become free mature spermatozoa in the lumen of seminiferous tubules.

Human spermiogenesis depicts particular features related to the uniqueness of human spermatozoa, including specific modifications of nuclear shape and chromatin structure, acrosome development, flagellar
growth, and formation of the mitochondrial sheath. Round euchromatic nuclei of early spermatids elongate while their chromatin progressively condenses, the Golgi-derived acrosome locates at the cephalic pole and spreads flat over the nucleus, the proximal centriole migrates and lodges at the caudal nuclear pole and the axoneme of the future sperm cell grows from the distal centriole and emerges into the extracellular space. These changes have been summarized in a series of eight steps.
Steps 1–2: Spermatid nuclei have finely granular chromatin with small non-prominent nucleoli. The Golgi complex, in a juxtanuclear location, has given rise to pro-acrosomic vesicles that contain dense granules and fuse into a large acrosomic vesicle that attaches to the nuclear membrane at the spermatid cranial pole. This vesicle flattens and spreads as a dense acrosome that will eventually cover between half and two-thirds of the nuclear surface. At these stages the centrioles migrate first to the cell membrane (where the axoneme grows from the distal centriole toward the extracellular space), and later to the caudal nuclear pole, where the proximal centriole lodges in a shallow concavity (the implantation fossa) defining the bipolar nature of the spermatozoon. Mitochondria, first located at the cell periphery, become randomly distributed on the caudal spermatid cytoplasm in step 2. At the neck region, around the proximal centriole, a dense striated structure develops that will become the connecting piece, a structure that fastens the tail to the sperm head.
Steps 3–5: The spermatid nucleus progressively elongates and flattens at the area covered by the acrosome while chromatin starts to condense by increasing the size and density of its granular components. Chromatin condensation starts at the tip of the head and progresses caudally, accompanied by a significant reduction of nuclear size and further flattening of the acrosome-covered area. The axoneme elongates and thickens by the addition of periaxonemal structures: the outer dense fibres and the fibrous sheath. The spermatid cytoplasm now occupies a distal position that anticipates the formation of the residual cytoplasm that will eventually disengage from the main sperm cell body at spermiation.
Steps 6–8: Nuclear elongation/flattening and chromatin condensation proceed to their mature stage. Mitochondria assemble around the first part of the axoneme to form the sperm midpiece. The residual cytoplasm further separates from the main cell body but remains attached to it by a slender stalk until mature spermatids are ready to be released into the lumen of seminiferous tubules as free spermatozoa.

The spermatid nucleus and the golgi complex; nuclear remodelling, chromatin compaction and acrosome development
During spermiogenesis, the organization of germ cell d DNA undergoes remarkable modifications. In early round spermatids e , DNA is associated with nuclear histones, forming a protein complex that organizes into
globular octamers by the association of a pair of each of the four histone components [H2A, H2B, H3 and H4]. These core particles are encircled by 146 DNA base pair filaments, forming nucleosomes, the basic structure of loosely bound DNA–histone complexes linearly assembled as beads in a string. This loose association is characteristic of euchromatin, prevalent in transcriptionally active somatic cells and germ cells up to early spermatids, and results in a dispersed microgranular and filamentous nuclear substructure. During spermiogenesis chromatin condensation starts when histones are removed and replaced by intermediate proteins and ultimately by protamines, smaller and structurally very different proteins that accommodate into minor DNA grooves and establish a strong bond that is further stabilized by cross-linking of disulphide bonds, resulting in very stable, highly compacted DNA. This spatial macromolecular organization renders DNA transcriptionally silent, but at the same time shields it and ensures its stability and resiliency to external influences during sperm transit. The process of DNA protamination–condensation is visualized through spermiogenesis as the evolution of dispersed chromatin into a progressively denser granular structure that leads to the highly compact chromatin of mature spermatozoa. 

Chromatin dynamics during spermiogenesis
The function of sperm is to safely transport the haploid paternal genome ( haploid = one copy of each chromosome ) to the egg containing the maternal genome. The subsequent fertilization leads to transmission of a new unique diploid genome to the next generation. Before the sperm can set out on its adventurous journey, remarkable arrangements need to be made. Haploid spermatids undergo extensive morphological changes, including a striking reorganization and compaction of their chromatin. Thereby, the nucleosomal, histone-based structure is nearly completely substituted by a protamine-based structure. This replacement is likely facilitated by incorporation of histone variants, post-translational histone modifications, chromatin-remodelling complexes, as well as transient DNA strand breaks.  Protamines are necessary to protect the paternal genome.  Hyperacetylation of histones just before their displacement is vital for progress in chromatin reorganization but is clearly not the sole inducer. In this review, we highlight the current knowledge on post-meiotic chromatin reorganization and reveal for the first time intriguing parallels in this process in Drosophila and mammals. 2 We now know that in many organisms spermiogenesis is accompanied by a dramatic reorganization of chromatin from a nucleosomal histone-based structure to a structure largely based on protamines. The replacement of histones by protamines is gradual. First, some of the canonical histones are replaced by testis-specific histone variants. Subsequently, so-called transition proteins are incorporated as nucleosomes are removed, and finally, protamines generate the tightly packaged sperm nucleus. In both flies and mammals, specific histone modifications and transient formation of DNA breaks precede or accompany protamine deposition. Over the past two decades, many chromatin components that specifically function during spermiogenesis have been described.

Germ cells mediate the transfer of genetic information from generation to generation and are thus pivotal for maintenance of life. Spermatogenesis is a continuous and precisely controlled process that leads to the formation of haploid sperm capable of fertilization. The process of spermatogenesis is highly conserved among many organisms and can be subdivided into three crucial phases: a mitotic amplification phase, a meiotic phase, and a post-meiotic phase also known as spermiogenesis. Germ cells in the post-meiotic phase can be subdivided into early spermatids with round nuclei, intermediate spermatids with elongating nuclei, and spermatids with condensed nuclei.  During spermiogenesis in both flies and mammals, round spermatids differentiate into mature sperm. During this process, the nuclear volume dramatically reduces, and histones are gradually replaced by protamines


Key chromatin remodeling events during spermiogenesis in mice and flies. 
Shortly after meiosis, spermatids are characterized by a round nucleus that elongates and reshapes during spermiogenesis. In parallel, the nucleosomal histone-based chromatin configuration is replaced by a mainly protamine-based tightly compacted structure. This chromatin reorganization is accompanied by hyperacetylation of histone H4 as well as the transient appearance of DNA breaks.

From histones to protamines
The process of spermatogenesis in mammals and in Drosophila species is similar, although the size and shape of mature sperm, as well as the time span for spermatogenesis, differ considerably. The testes of Drosophila and all mammalian species contain all stages of spermatogenesis, from stem cells to mature sperm, and spermatogenesis occurs within a tubular structure. Germ cells develop in close contact with the surrounding somatic cells, known as cyst cells in Drosophila and Sertoli cells in mammals. In mammals, the number of stages that can be observed varies among species. 

Protamines stabilize sperm chromatin by their assembly in the minor groove of DNA into densely packed arrays linked by intermolecular and intramolecular disulfide bonds. In addition, protamine deficiencies are associated with infertility in men, and the frequency of human sperm with DNA damage correlates with failure of embryonic development. 3  A reduction in the amount of protamine would change not only the stoichiometry of the major components of the chromatin but also the net charge in the sperm nucleus, thereby affecting chromatin condensation and stability.

Fertilization involves a direct interaction amongst spermatozoa and oocytes, a merger of the cell membrane, and a union of male and female gamete genome. The process can thoroughly take place when supported by the compact spermatozoa DNA integrity. Spermatozoa's DNA integrity plays a significant role in delivering accurate genetic information. 6 The compactness of spermatozoa chromatin is due to the bonding between DNA and proteins of core spermatozoa, particularly the protamine. A number of causes why spermatozoa DNA damages are the protamine deficiency. Protamine plays an important role in male's normal fertility. The deficiency in P1 and P2 causes subfertile or severe infertile condition.

The human sperm nucleus contains two types of protamine: protamine 1 (P1) encoded by a single-copy gene and the family of protamine 2 (P2) proteins (P2, P3 and P4), all also encoded by a single gene that is transcribed and translated into a precursor protein. 7 Their function goes from condensation of the sperm nucleus into a compact hydrodynamic shape, protection of the genetic message delivered by the spermatozoa, involvement in the processes maintaining the integrity and repair of DNA during or after the nucleohistone–nucleoprotamine transition and involvement in the epigenetic imprinting of the spermatozoa. 

The protamine family of sperm nuclear proteins
The protamines are a diverse family of small proteins that are synthesized in the late-stage spermatids of many animals and plants and bind to DNA, condensing the spermatid genome into a genetically inactive state. The two protamines found in mammals, P1 and P2, are the most widely studied. P1 packages sperm DNA in all mammals, whereas protamine P2 is present only in the sperm of primates, many rodents and a subset of other placental mammals. P2, but not P1, is synthesized as a precursor that undergoes proteolytic processing after binding to DNA. Both P1 and P2 have been shown to be required for normal sperm function in primates and many rodents.

Comparisons of the amino-acid sequences of vertebrate and invertebrate protamines show that the protamines from all animals do not constitute a true family

My comment: Of course, thats a major headage for evolutionary biologists. To overcome the problem, the "ad-hoc" explanation is:

the sequence, structure, and possibly function of protamines  evolved independently in vertebrates and various invertebrate groups (mollusks, cephalopods and tunicates).

Hum... Really?!!

Two structural elements have been identified in all vertebrate protamines. One is a series of small 'anchoring' domains containing multiple arginine or lysine amino acids (three or more per domain, highlighted in red in the figures in Additional data file 1) that are used to bind the protein to DNA. The protamines present in eutherian mammals all contain multiple cysteine residues that are oxidized to form disulfide bridges that link the protamines together and stabilize the chromatin complex during the final stages of sperm maturation.

Upon binding to DNA, P1 wraps around the DNA helix in the major groove with one protamine molecule being bound per turn of DNA helix.


Protamine molecules bind in the major groove of DNA, neutralizing the phosphodiester backbone of DNA and causing the DNA molecules to coil into toroidal structures.
(a) Model showing how two adjacent salmon protamine molecules (blue atoms) wrap around the DNA helix (white atoms) and bind within the major groove of DNA.
(b) Scanning-probe images of toroidal DNA-protamine complexes prepared in vitro on a graphite surface by adding protamine to DNA attached loosely to the surface. The toroids formed in vitro are similar in size and shape to those isolated from human sperm chromatin
(c). (c) Scanning-probe microscope images of native DNA-protamine toroids obtained from human sperm chromatin. These toroids, which comprise the basic subunit structure of protamine-bound DNA, contain approximately 50,000 bp of DNA coiled into each donut-shaped structure.

Transition proteins: transiently expressed non-histone chromatin components in spermatids
Between histone removal and protamine deposition in mammalian spermatids, about 90% of the basic chromatin components consists of transition proteins. Mouse transition protein 1 (TP1) and 2 (TP2), encoded by Tnp1 and Tnp2, are arginine- and lysine-rich proteins that bind strongly to DNA. TP1 decreases the melting temperature of DNA, relaxes the DNA in nucleosomal core particles, and stimulates the DNA-relaxing activity of topoisomerase I, which indicates that TPs could help chromatin remodelling by making the DNA more flexible. However, others have reported that neither TP1 nor TP2 is able to cause topological changes in supercoiled DNA. In addition, it has been proposed that the TPs can mediate DNA and chromatin condensation. Finally, TP1 has been found to stimulate repair of single-strand DNA breaks. Tnp1 knockout in mice leads to severely reduced sperm motility and to elevated levels of TP2 and of some protamine 2 precursors in spermatid nuclei that might partially compensate for the lack of TP1. About 60% of Tnp1-deficient males is sterile. In contrast, Tnp2- deficient mice are fertile and display only mild sperm abnormalities. In mice lacking both TPs, histone displacement and protamine deposition proceed relatively normally, while chromatin condensation is irregular in all spermatids. Furthermore, many late spermatids show DNA breaks, the number of epididymal sperm is drastically reduced, and mice are sterile. There is some functional redundancy between TP1 and TP2, and that they are not required for histone removal and protamine loading, yet are important for the proper regulation of chromatin structure. 

Protamines and chromatin components of mature sperm chromatin
Transition proteins are subsequently replaced by the highly basic protamines in late spermatids. Mammalian protamines are arginine- and cysteine-rich proteins with a low molecular mass and are associated with DNA in late spermatids and mature sperm. Most mammalian species have only one type of protamine present in sperm, while the genomes of mice and humans encode two protamine types: Protamine 1 (PRM1 or P1) and Protamine 2 (PRM2 or P2). Whereas protamines of the P2 family (P2, P3, and P4), which differ only in the N-terminal extension of 1–4 residues, are generated by proteolysis from a precursor encoded by a single gene, protamine 1 is synthesized as a mature protein. Just as in mice and humans, also the genome of Drosophila encodes two different protamines. These protamines, ProtA and ProtB (encoded by Mst35Ba and Mst35Bb, respectively), are cysteine-rich but less arginine-rich than mammalian P1 and P2. In mice, PRM1 and PRM2 are essential for male fertility, and even deletion of a single copy of either Prm1 or Prm2 leads to infertility. In humans, nuclei of normal sperm cells contain similar amounts of protamine 1 and 2 (P1/P2 ratio of 1); deviations from this ratio correlate with male infertility. Surprisingly, in Drosophila, ProtA and ProtB are not essential for fertility; when both protamines are missing, only about 20% of the sperm nuclei displays abnormal morphology. However, one has to consider that these two protamines are not the only chromatin components of sperm in flies. The HILS1- like protein Mst77F marks distinct chromatin regions within sperm nuclei, and its deposition is independent of the incorporation of protamines. It needs to be clarified whether further chromatin components exist in mature sperm that might be functionally redundant with protamines.

In spermiogenesis, the majority of the core histones are replaced sequentially, first by transition proteins and then protamines, facilitating chromatin hyper-compaction. 1 In this histone-to-protamine transition process epigenetic regulators interact with each other to remodel chromatin architecture. Testis-specific transcription factors play a critical role in controlling the haploid-specific developmental program, recent studies underscore the essential functions of epigenetic players involved in the dramatic genome remodeling that takes place during wholesale histone replacement. Histone variants and histone writers/readers/erasers, rewire the haploid spermatid genome to facilitate histone substitution by protamines in mammals. During spermatid development, the paternal genome is re-organized and packaged into highly condensed nuclei of the spermatozoa. One of the dramatic changes that occurs lies in the transition from nucleosome-based chromatin to protamine-based chromatin arrays, which facilitates the condensation of sperm heads and protects the paternal DNA from damage and mutagenesis. 

Epigenetics, referring to the phenotypic inheritance of traits in the progeny without altering the genetic DNA code, is involved in a wide range of biological processes, including germ cell development. They undergo global genome-wide de novo reprogramming mainly orchestrated by the DNA demethylases and methyltransferases, such as ten-eleven translocation proteins (TET1/2) and DNMT3A/B, which induce the active DNA de-methylation and methylation, respectively, in both the male and female primordial germ cell populations.

Histone modifications that precede histone removal during spermiogenesis
During spermiogenesis, most histones are replaced by transition proteins and subsequently by protamines. This drastic alteration in chromatin configuration is expected to require mechanisms to promote eviction of nucleosomes in favor of incorporation of transition proteins, followed by a subsequent exchange of transition proteins for protamines. In addition to the incorporation of histone variants, specific histone modifications also affect the higher-order chromatin structure and play important roles in gene regulation and maintenance of genome integrity. Histones are commonly post-translationally modified at the amino-terminal tails. The most-studied histone modifications include acetylation, methylation, phosphorylation, ubiquitination, and SUMOylation. These modifications can be recognized by proteins and facilitate downstream events on chromatin, resulting in a more open or closed chromatin configuration. In both flies and mammals, hyperacetylation of histone H4 has been observed in elongating spermatids just prior to histone removal.  H4 hyperacetylation in mammalian spermatids leads to an open chromatin structure that facilitates and induces histone displacement. In mice and humans, reduced levels of histone H4 hyperacetylation in sperm correlates with impaired fertility. Previously established testis organ cultures have enabled us to address the functional importance of histone hyperacetylation in Drosophila. Indeed, inhibition of histone acetyltransferases (HATs) in in vitro cultures of Drosophila testes leads to spermiogenesis arrest, and the chromatin remains in a histone-based configuration. Thus, hyperacetylation appears to be a prerequisite for proper chromatin reorganization. However, premature acetylation does not induce premature chromatin reorganization in Drosophila, which suggests that H4 hyperacetylation is not the sole inducer of chromatin remodelling.

Expression of different histone methyltransferases and demethylases has been observed during spermatid elongation in flies and mammals. This coexistence of both types of enzymes might be crucial to balance regions of “opened”
and “closed” chromatin. 

Insights into the mechanisms of chromatin reorganization during spermiogenesis
The histone-to-protamine transition, require mechanisms to access DNA. These mechanisms often require one or more  covalent histone modifications and histone replacement by histone variants. In addition, ATP-dependent chromatin remodelling complexes often participate in gaining DNA accessibility.The mechanisms that potentially lead to the mainly protamine-based DNA packaging in mature sperm are schematically summarized within a model.


Model of the regulatory mechanisms that may lead from a nucleosomal-based to a mainly protamine-based chromatin configuration. 
(A) Increased levels of histone acetyltransferases mediate hyperacetylation of histones to obtain a more open chromatin structure. This process might be supported by specific degradation of histone deacetylases. In parallel, chaperones participate in incorporation of histone variants to loosen the nucleosomal structure. Exchanged canonical histones, in turn, may undergo poly-ubiquitination and become degraded through proteasomes
(B) Binding of bromodomain proteins to acetyl-residues may facilitate recruitment of chromatin-remodelling complexes to further relax chromatin. This is accompanied by the induction of DNA strand breaks. The relaxed chromatin configuration allows replacement of histones by transition proteins, possibly with the help of molecular chaperones. Subsequently, DNA damage repair mechanisms must act to ensure chromatin integrity. 
(C) Finally, molecular chaperones most likely aid in replacement of transition proteins by protamines to allow tight packaging of DNA into a higher-order structure. Transition proteins may become degraded through poly-ubiquitination and proteasome activity. Note that residual histones are not depicted.

To date, no ATP-dependent chromatin-remodelling complexes have been described in post-meiotic male germ cells. Nevertheless, in rat, the ATPase subunits of the ATP-dependent remodelling complex SWI/ SNF, Smarca2/Brm and Smarca4/Brg-1, are highly expressed in round spermatids. In addition, high expression levels of the SWI/SNF subunit Smarce1/BAF57 have been observed in round spermatids. The protein Spermatogenic cell HDAC-interacting protein 1 (SHIP1) is expressed in the nuclei of spermatocytes and round spermatids before hyperacetylation of histone H4, and SHIP1 is a component of a complex with chromatin-remodelling activity. Thus, SHIP1 and SWI/SNF chromatin-remodelling complexes might assist in chromatin reorganization during spermiogenesis. In addition, transition proteins themselves might help to remodel chromatin. However, in mice, apart from a putative role in histone removal, these remodelers may also aid in the global repression of gene transcription that occurs during this phase of spermiogenesis. Still, based on the currently available data, it appears most likely that a chromatin-remodelling complex might guide the replacement of histones by transition proteins during spermatid differentiation.

The process of chromatin reorganization in spermatids most likely also requires mechanisms to incorporate histone variants, transition proteins, and protamines. In addition, mechanisms to remove histones and transition proteins have to exist. Chromatin assembly is mediated by histone chaperones and ATP-utilizing motor proteins. Histone chaperones function in histone removal as well as histone exchange and that they team up with ATP-dependent chromatin-remodelling factors. Molecular chaperones are required to remove histones and at the same time aid in incorporating transition proteins and protamines into spermatid chromatin.

After fertilization: back to histones
The fusion of the oocyte and the sperm entails resumption ofmeiosis of the oocyte and formation of the male pronucleus. Directly after the release of the sperm nucleus into the oocyte cytoplasm, protamines are quickly replaced by maternally supplied histones. In addition, testis-specific histone variants rapidly disappear from the paternal genome after fertilization. The treatment of hamster eggs with antimycin A prevents paternal chromatin remodeling, which suggests that ATP-dependent processes are required for protamine replacement. It has been reported that in Xenopus laevis, the chaperone nucleoplasmin (NPM) is involved in histone assembly onto the paternal chromatin. In mammals, NPM1, NPM2, and NPM3 members of the nucleoplasmin/nucleophosmin (NPM) family are expressed in oocytes, and  they regulate sperm chromatin decondensation. Moreover, in NPM2-deficient mice, early embryogenesis is severely impaired. Additionally, the Drosophila proteins nucleosome assembly protein-1 (dNAP-1) and DF31 as well as the human Template activating factor I (TAF-I) have been shown to promote decondensation of sperm chromatin. In Drosophila, the maternal effect embryonic lethal mutation sésame (ssm) affects male pronucleus formation but not protamine removal. ssm is a point mutation in the Hira gene that encodes the H3.3 histone chaperone HIRA. HIRA is essential for decondensation of the sperm nucleus and nucleosome assembly . Eggs laid by Hiradeficient females lose the paternal chromosomes and produce gynogenic haploid embryos.

Recently, it has been proposed that HIRA cooperates with Yemanuclein to establish the H3.3-containing nucleosome in the male nucleus at fertilization. Also in mouse zygotes, a strong enrichment of H3.3 as well as HIRA expression has been observed, which indicates that the function of HIRA in the protamine-to-histone transition may be conserved from flies to mammals.





Summary of events leading to the fusion of egg and sperm cell membranes in sea urchin fertilization, which is external.
(1) The sperm is chemotactically attracted to and activated by the egg. 
(2, 3) Contact with the egg jelly triggers the acrosome reaction, allowing the acrosomal process to form and release proteolytic enzymes. 
(4) The sperm adheres to the vitelline envelope and lyses a hole in it. 
(5) The sperm adheres to the egg cell membrane and fuses with it. The sperm pronucleus can now enter the egg cytoplasm.

Two major mechanisms use species-specific sperm attraction and species-specific sperm activation.

The acrosome reaction
The acrosome plays a crucial role in the recognition and penetration of the egg at the time of fertilization. Globozoospermia is diagnosed when all spermatozoa are round-headed and lack acrosomes. This defect is genetic in origin and originates in spermiogenesis, specifically during acrosome formation and sperm head elongation. The chromatin compaction appears to be disturbed. Affected males suffer from reduced fertility or even infertility.

In most marine invertebrates, the acrosome reaction has two components: the fusion of the acrosomal vesicle with the sperm cell membrane (an exocytosis that results in the release of the contents of the acrosomal vesicle), and the extension of the acrosomal process. The acrosome reaction in sea urchins is initiated by contact of the sperm with the egg jelly. Contact causes the exocytosis of the sperm’s acrosomal vesicle. The proteolytic enzymes and proteasomes (protein-digesting complexes) thus released digest a path through the jelly coat to the egg cell surface. Once the sperm reaches the egg surface, the acrosomal process adheres to the vitelline envelope and tethers the sperm to the egg. It is possible that proteasomes from the acrosome coat the acrosomal process, allowing it to digest the vitelline envelope at the point of attachment and proceed toward the egg. In sea urchins, the acrosome reaction is initiated by sulfate-containing polysaccharides in the egg jelly that bind to specific receptors located directly above the acrosomal vesicle on the sperm cell membrane. These polysaccharides are often highly speciesspecific, and egg jelly factors from one species of sea urchin generally fail to activate the acrosome reaction even in closely related species. Thus, activation of the acrosome reaction serves as a barrier to interspecies (and thus unviable) fertilizations. This is important when numerous species inhabit the same habitat and when their spawning seasons overlap.

Sperm attraction: Action at a distance
Species-specific sperm attraction has been documented in numerous species, including cnidarians, mollusks, echinoderms, amphibians, and urochordates. In many species, sperm are attracted toward eggs of their species by chemotaxis—that is, by following a gradient of a chemical secreted by the egg. These oocytes control not only the type of sperm they attract, but also the time at which they attract them, releasing the chemotactic factor only after they reach maturation. The mechanisms of chemotaxis differ among species, and chemotactic molecules are different even in closely related species. In sea urchins, sperm motility is acquired only after the sperm are spawned. As long as sperm cells are in the testes, they cannot move because their internal pH is kept low (about pH 7.2) by the high concentrations of CO2 in the gonad. However, once sperm are spawned into seawater, their pH is elevated to about 7.6, resulting in the activation of the dynein ATPase. The splitting of ATP provides the energy for the flagella to wave, and the sperm begin swimming vigorously.

a

b The acrosome is an organelle that develops over the anterior half of the head in the spermatozoa (sperm cells) of many animals including humans. It is a cap-like structure derived from the Golgi apparatus. Acrosome formation is fully completed 5–10 years after testicular maturation. In Eutherian mammals the acrosome contains digestive enzymes. These enzymes break down the outer membrane of the ovum, called the zona pellucida, allowing the haploid nucleus in the sperm cell to join with the haploid nucleus in the ovum.

c


d A germ cell is any biological cell that gives rise to the gametes of an organism that reproduces sexually. In many animals, the germ cells originate in the primitive streak and migrate via the gut of an embryo to the developing gonads. There, they undergo meiosis, followed by cellular differentiation into mature gametes, either eggs or sperm. 4

e The spermatid is the haploid male gametid that results from division of secondary spermatocytes. As a result of meiosis, each spermatid contains only half of the genetic material present in the original primary spermatocyte. 5


1. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4896072/
2. http://sci-hub.tw/https://www.ncbi.nlm.nih.gov/pubmed/24091090/
3. https://academic.oup.com/biolreprod/article/69/1/211/2712972
4. https://en.wikipedia.org/wiki/Germ_cell
5. https://en.wikipedia.org/wiki/Spermatid
6. https://www.sciencedirect.com/science/article/pii/S2305050016300914
7. http://sci-hub.tw/https://www.ncbi.nlm.nih.gov/pubmed/16581810

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7 Rocket science at its best on Sun Dec 23, 2018 1:40 pm

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Rocket science & Sex

this article is best read at my library:
http://reasonandscience.catsboard.com/t1685-sex-the-queen-of-problems-in-evolutionary-biology#6390

Imagine that Elon Musks Space X rocket-spaceship had to transport a precious cargo from planet Earth to Mars. In order to do so, Space X had to be purposefully built for the mission.  The cargo had to be compacted into the smallest possible and volume and protected from Outer Space in order to arrive secure and unharmed on its destination. Specialized robots would put the cargo on constant surveillance during the whole trip, and if for some reason, during the transport, the cargo would be harmed, immediately repair Robots would be recruited to fix the problem, to make sure, that the cargo arrives fully intact at its destination. On Mars, there would be a protective wall. In order to get in and deliver the cargo, the Rocket would be capped purposefully with material harder than steel to break through the protective wall, get inside, and there, the Cargo would arrive at its destination. As soon as the Rocket goes through, the protective wall hardens so much, that if any other Spaceship would try to penetrate it too, it would not succeed. If a second rocket would succeed to get in the wall, it would mean catastrophic failure. On place, specific complex machinery would be waiting to unpack the precious good: a hard disk, which would be inserted into a computer,  and then its information content extracted and used to build an entirely new civilisation, with machines, buildings, factories, machines, computers, and so on. If any of the stages of the transport were not correctly programmed and implemented, or surveillance failing, the transport would not succeed. If any of the stages of the processes failed, the mission would not be accomplished. 

Earth is the male, Mars is the female, the Rocket is the male sperm, and the cargo is the Chromosomes which travel from male to female. the sperm penetrates the egg, and fertilization occurs. No other sperm can penetrate the egg, or fertilization cannot occur. Fertilization is an awe-inspiring, incomparably more complex process than anything invented by Elon Musk, or mankind at large.

Fertilization is of amazing complexity: A sperm cell has to be matured. Spermatogenesis begins with a single cell that undergoes a dramatic transformation, culminating with the hypercompaction of DNA into the sperm head by replacing histones with protamines

Nucleosomes function and design
http://reasonandscience.catsboard.com/t2051-nucleosomes-function-and-design

Histones function and design
http://reasonandscience.catsboard.com/t2050-histones-function-and-design

Chromosome condensation and compaction is nothing short than awe-inspiring, amazing evidence of setup by a supreme intelligence.  
http://reasonandscience.catsboard.com/t2086-chromosome-condensation-amazing-evidence-of-design

When the sperm is mature and reaches the egg, a complex dialogue takes place between egg and sperm. The egg activates the sperm metabolism that is essential for fertilization, and the sperm reciprocates by activating the egg metabolism needed for the onset of development. This is an irreducible process, where all players must be in place to perfom their job. 

Fertilization
Fertilization is the process where sperm and egg—fuse together to begin the creation of a new organism. Fertilization accomplishes the combining of genes derived from two parents and reproduction - the generation of a new organism. Thus, the first function of fertilization is to transmit genes from parent to offspring, and the second is to initiate in the egg cytoplasm those reactions that permit development to proceed.  During fertilization, the egg and sperm must meet, the genetic material of the sperm must enter the egg, and the fertilized egg must initiate cell division and the other processes of development. Sperm and egg must travel toward each other, and chemicals from the eggs can attract the sperm. Gamete recognition occurs when proteins on the sperm cell membrane meet proteins on the extracellular coating of the egg. In preparation for this meeting, the sperm cell membrane is altered significantly. The sperm and egg pronuclei travel toward one another and the genetic material of the gametes combines to form the diploid chromosome content carrying the genetic information for the development of a new organism.

Each sperm cell consists of a  nucleus, a propulsion system to move the nucleus, and a sac of enzymes that enable the nucleus to enter the egg. In most species, almost all of the cell’s cytoplasm is eliminated during sperm maturation, leaving only certain organelles that are modified for spermatic function. During the course of maturation, the sperm’s haploid nucleus becomes very streamlined and its DNA becomes tightly compressed. 

Spermiogenesis: the differentiation of the sperm
The production of mature and motile sperm is a detailed process that utilizes many molecular players to ensure the faithful execution of spermatogenesis. Precise execution of the stages of spermatogenesis results in the production of motile sperm. Spermatogenesis is a highly orchestrated process that requires the correct interplay and timing of all molecular constituents to produce fully functional and motile sperm. Defects in spermatogenesis can impact a male’s overall fitness, which encompasses the ability to both survive and reproduce successfully. Aberrations during any stage within spermatogenesis can have profound effects on sperm quantity, motility, morphology and ability to fertilize an egg. In addition, poor packaging of chromatin within sperm nuclei can reduce the protection of DNA against chemical and physical damage, potentially leading to mutations and unfit offspring. Modifications to sperm chromatin require the use of specialized DNA-binding proteins, referred to as protamines, which are capable of achieving the level of organization and compression necessary to fit the haploid genome into the compact sperm head.

The mammalian haploid spermatid is a roundunflagellated cell that looks nothing like the mature vertebrate sperm. The next step in sperm maturation, then, is spermiogenesis, the differentiation of the sperm cell. For fertilization to occur, the sperm has to meet and bind with an egg, and spermiogenesis prepares the sperm for these functions of motility and interaction. In many organisms, male germ cells undergo a series of morphological transformations during spermiogenesis to build a sperm with its typical species-specific shape from an initially round cell.

Chromatin condensation starts when histones are removed and replaced by intermediate proteins and ultimately by protamines, smaller and structurally very different proteins that accommodate into minor DNA grooves and establish a strong bond that is further stabilized by cross-linking of disulphide bonds, resulting in very stable, highly compacted DNA. This spatial macromolecular organization renders DNA transcriptionally silent, but at the same time shields it and ensures its stability and resiliency to external influences during sperm transit. 

Each day, some 100 million sperm are made in each human testicle, and each ejaculation releases 200 million sperm. Unused sperm are either resorbed or passed out of the body in urine.

From histones to protamines
Fertilization involves a direct interaction amongst spermatozoa and oocytes, a merger of the cell membrane, and a union of male and female gamete genome. The process can thoroughly take place when supported by the compact spermatozoa DNA integrity. Spermatozoa's DNA integrity plays a significant role in delivering accurate genetic information. The compactness of spermatozoa chromatin is due to the bonding between DNA and proteins of core spermatozoa, particularly the protamine. A number of causes why spermatozoa DNA damages are the protamine deficiency. Protamine plays an important role in male's normal fertility. Protamines stabilize sperm chromatin by their assembly in the minor groove of DNA into densely packed arrays linked by intermolecular and intramolecular disulfide bonds. In addition, protamine deficiencies are associated with infertility in men, and the frequency of human sperm with DNA damage correlates with failure of embryonic development. In addition, mechanisms to remove histones and transition proteins have to exist. Chromatin assembly is mediated by histone chaperones and ATP-utilizing motor proteins. Histone chaperones function in histone removal as well as histone exchange and that they team up with ATP-dependent chromatin-remodelling factors. Molecular chaperones are required to remove histones and at the same time aid in incorporating transition proteins and protamines into spermatid chromatin.  A reduction in the amount of protamine would change the net charge in the sperm nucleus, thereby affecting chromatin condensation and stability. During spermiogenesis, most histones are replaced by transition proteins and subsequently by protamines. This drastic alteration in chromatin configuration is expected to require mechanisms to promote eviction of nucleosomes in favor of incorporation of transition proteins, followed by a subsequent exchange of transition proteins for protamines.
 
The protamine family of sperm nuclear proteins
The protamines are small proteins that are synthesized in the late-stage spermatids of many animals and plants and bind to DNA, condensing the spermatid genome into a genetically inactive state. Comparisons of the amino-acid sequences of vertebrate and invertebrate protamines show that the protamines from all animals do not constitute a true family

My comment: Of course, that's a major headage for evolutionary biologists to explain their evolutionary origins. To overcome the problem, the "ad-hoc" explanation is: 

The sequence, structure, and possibly function of protamines evolved independently in vertebrates and various invertebrate groups (mollusks, cephalopods and tunicates).

Hum... Really?!!

Two structural elements have been identified in all vertebrate protamines. One is a series of small 'anchoring' domains containing multiple arginine or lysine amino acids (three or more per domain, highlighted in red in the figures in Additional data file 1) that are used to bind the protein to DNA. The protamines present in eutherian mammals all contain multiple cysteine residues that are oxidized to form disulfide bridges that link the protamines together and stabilize the chromatin complex during the final stages of sperm maturation.

Upon binding to DNA, P1 wraps around the DNA helix in the major groove with one protamine molecule being bound per turn of DNA helix. 

In spermiogenesis, the majority of the core histones are replaced sequentially, first by transition proteins and then protamines, facilitating chromatin hyper-compaction.  In this histone-to-protamine transition process epigenetic regulators interact with each other to remodel chromatin architecture. Recent studies underscore the essential functions of epigenetic players involved in the dramatic genome remodelling that takes place during wholesale histone replacement. Histone variants and histone writers/readers/erasers, rewire the haploid spermatid genome to facilitate histone substitution by protamines in mammals. During spermatid development, the paternal genome is re-organized and packaged into highly condensed nuclei of the spermatozoa.  The transition from nucleosome-based chromatin to protamine-based chromatin arrays, which facilitates the condensation of sperm heads and protects the paternal DNA from damage and mutagenesis. 

Epigenetics, referring to the phenotypic inheritance of traits in the progeny without altering the genetic DNA code, is involved in a wide range of biological processes, including germ cell development. They undergo global genome-wide de novo reprogramming mainly orchestrated by the DNA demethylases and methyltransferases, such as ten-eleven translocation proteins (TET1/2) and DNMT3A/B, which induce the active DNA de-methylation and methylation, respectively, in both the male and female primordial germ cell populations.

After fertilization: back to histones
The fusion of the oocyte and the sperm entails resumption of meiosis of the oocyte and formation of the male pronucleus. Directly after the release of the sperm nucleus into the oocyte cytoplasm, protamines are quickly replaced by maternally supplied histones. In addition, testis-specific histone variants rapidly disappear from the paternal genome after fertilization. ATP-dependent processes are required for protamine replacement. Chaperone nucleoplasmin (NPM) is involved in histone assembly onto the paternal chromatin. In mammals, nucleoplasmin is expressed in oocytes, and they regulate sperm chromatin decondensation. Moreover, HIRA protein is essential for decondensation of the sperm nucleus and nucleosome assembly.[/size]

It is evident that such a complex process could not emerge gradually, but had to be implemented fully working, right from the beginning.

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8 Spermatogenesis, by evolution, or design? on Tue Dec 25, 2018 11:37 am

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Spermatogenesis, by evolution, or design?

http://reasonandscience.catsboard.com/t1685-sex-the-queen-of-problems-in-evolutionary-biology#6400

Confronted with the arguments of a proponent of evolution, one of the first questions appropriate to ask is, similar to the chicken-egg dilemma: In sexual reproduction, what evolved first, the egg, or the sperm?

Fertilization is of amazing complexity: A sperm cell has to be matured. Spermatogenesis begins with a single cell that undergoes a dramatic transformation, culminating with the hypercompaction of DNA through chromatin comdensation into the sperm head by replacing histones with protaminesChromatin condensation starts when histones are removed and replaced by intermediate proteins and ultimately by protamines, smaller and structurally very different proteins that accommodate into minor DNA grooves and establish a strong bond that is further stabilized by cross-linking of disulphide bonds, resulting in very stable, highly compacted DNA. Histone chaperone helper proteins function in histone removal as well as histone exchange and that they team up with ATP-dependent chromatin-remodelling factors. Molecular chaperones are required to remove histones and at the same time aid in incorporating transition proteins and protamines into spermatid chromatin.  This spatial macromolecular organization renders DNA transcriptionally silent, but at the same time shields it and ensures its stability and resiliency to external influences during sperm transit. Spermatozoa's DNA integrity plays a significant role in delivering accurate genetic information. Protamine deficiencies are associated with infertility in men, and the frequency of human sperm with DNA damage correlates with failure of embryonic development. In addition, mechanisms to remove histones and transition proteins have to exist. The fusion of the oocyte and the sperm entails resumption of meiosis of the oocyte and formation of the male pronucleus. Directly after the release of the sperm nucleus into the oocyte cytoplasm, protamines are quickly replaced by maternally supplied histones. In addition, testis-specific histone variants rapidly disappear from the paternal genome after fertilization. ATP-dependent processes are required for protamine replacement. Chaperone nucleoplasmin (NPM) is involved in histone assembly onto the paternal chromatin. Moreover, HIRA protein is essential for decondensation of the sperm nucleus and nucleosome assembly.

Question: Since MATERNALLY SUPPLIED histones replace protamines, is that not an interdependent process, and orchestrated like teamwork, where the male sperm undergoes life essential transformation,  where histones are replaced with protamines, and the female oocyte supplies the histones to replace protamines, and as such, both had to be fully set up and operating, and the whole process of fertilization be working from day one?  Consider as well, that my description above is extremely simplified.

In reality, many essential, irreducible players are working together in a detailed process that utilizes many molecular players to ensure the faithful execution of spermatogenesis. Precise execution of the stages results in the production of motile sperm. Spermatogenesis is a highly orchestrated process that requires the correct interplay and timing of all molecular constituents to produce fully functional and motile sperm. Defects in spermatogenesis can impact a male’s overall fitness, which encompasses the ability to both survive and reproduce successfully. Aberrations during any stage within spermatogenesis can have profound effects on sperm quantity, motility, morphology and ability to fertilize an egg. In addition, poor packaging of chromatin within sperm nuclei can reduce the protection of DNA against chemical and physical damage, potentially leading to mutations and unfit offspring. Modifications to sperm chromatin require the use of specialized DNA-binding proteins, referred to as protamines, which are capable of achieving the level of organization and compression necessary to fit the haploid genome into the compact sperm head.

Consider how many essential players are required to go from a nucleosomal-based to a mainly protamine-based chromatin configuration:

- Histone acetyltransferases
- Chaperones
- Proteasomes.
- Bromodomain proteins
- Chromatin-remodelling complexes
- Transition proteins
- Molecular chaperones
- DNA damage repair mechanisms
- Protamines
- Histone Variants
- Molecular Chaperone
- Ubiquitin
- Poly-Ubiquitin
- Histone Deacetylase
- Histone Acetyltransferase
- BromodomainProtein
- DNA Strand Break Induction proteins
- Chromatin- Remodeling Complex
- DNA Repair enzymes
- Proteasome
- T Transition Protein P Protamine
- E2-Conjugating Enzymes
- Canonical Nucleosome
  
If one of these parts is missing, Spermatogenesis cannot occur properly, and fertilization cannot succeed. I suppose above makes it clear enough, why fertilization and sexual reproduction is considered by biologists the QUEEN problem of evolutionary biology ?!!!

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What evolved first: Sex as biological function, or the desire of sex, and the attractiveness of the opposed sexes? What if male and female evolved, but sexual preference would be mostly for the same sex? Sexual reproduction in animals and plants is btw. far more prevalent than asexual reproduction, and there is no scientific explanation, why. Even bacteria reproduce by parasexual reproduction. Also, by evolutionary logic, how can the jungle of diverse courtship and mating strategies that we find in nature be explained ? Why are most flowering plants, but only a few animals, hermaphroditic? Why is it that mostly males compete for females, and not the other way around? These questions are puzzling for evolutionary biologists, and all that is, is the hope that one day, science will find answers. Until that happens, the gaps are filled with naturalism. Naturalism of the gaps.

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Understanding the evolution of anisogamy in the early diverging fungus, Allomyces
December 08, 2017
Although adaptive explanations for the evolution of anisogamy abound, we lack comparable insights into molecular changes that bring about the transition from monomorphism to dimorphism.

https://www.biorxiv.org/content/early/2017/12/08/230292

Wiki: Evolution of anisogamy:
the last of these three is not well supported
assume
assumed
mathematical theory proposed
this model assumed
would lead
If it is assumed
these early models assume
became widely accepted
where it seems
Theory also suggests
could only have
relatively sound theory
would
it has also been claimed
valuable model system
https://en.wikipedia.org/wiki/Anisogamy#Evolution



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