In order to explain the origin of the Cambrian animals, one must account not only for new proteins and cell types, but also for the origin of new body plans . . . Mutations in genes that are expressed late in the development of an organism will not affect the body plan. Mutations expressed early in development, however, could conceivably produce significant morphological change (Arthur 1997:21) . . . [but] processes of development are tightly integrated spatially and temporally such that changes early in development will require a host of other coordinated changes in separate but functionally interrelated developmental processes downstream. For this reason, mutations will be much more likely to be deadly if they disrupt a functionally deeply-embedded structure such as a spinal column than if they affect more isolated anatomical features such as fingers (Kauffman 1995:200) . . . McDonald notes that genes that are observed to vary within natural populations do not lead to major adaptive changes, while genes that could cause major changes--the very stuff of macroevolution--apparently do not vary. In other words, mutations of the kind that macroevolution doesn't need (namely, viable genetic mutations in DNA expressed late in development) do occur, but those that it does need (namely, beneficial body plan mutations expressed early in development) apparently don't occur.6 [Emphases added. Cf a more easily readable (and also peer-reviewed) but longer discussion, with illustrations, here.]
Now, this analysis highlights a significant distinction we need to make: micro-evolutionary changes are late-developing, and do not affect the core body plan and its associated functions. Such mutations are indeed possible and are observed. But, when the mutations get to the fundamental level of changing body plans -- i.e. macro-evolution -- they face the implication that we are now disturbing the core of a tightly integrated system, and so the potential for destructive change is much higher. Consequently, the genes that control such core features are stabilised by a highly effective negative feedback effect: random changes strongly tend to eliminate themselves through loss of integrity of vital body functions.
In response, it is often claimed that sufficient microevolution accumulates across time to constitute macroevolution. But, what we "see" in the fossil record of the Cambrian rocks is just that innovation at the core levels coming first, and coming massively -- just the opposite of what the NDT model would lead us to expect. For, as Dan Peterson summarises in his recent article:
To take just one example, a well-known (and unsolved) problem for Darwinism is the Cambrian Explosion. As noted by Stephen Meyer in the book Debating Design, this event might be better called the Cambrian Information Explosion. For the first three billion years of life on Earth, only single-celled organisms such as bacteria and bluegreen algae existed. Then, approximately 570 million years ago, the first multi-cellular organisms, such as sponges, began to appear in the fossil record. About 40 million years later, an astonishing explosion of life took place. Within a narrow window of about 5 million years, "at least nineteen and perhaps as many as 35 phyla (of 40 total phyla) made their first appearance on Earth...." Meyer reminds us that "phyla constitute the highest categories in the animal kingdom, with each phylum exhibiting unique architecture, blueprint, or structural body plan." These high order, basic body plans include "mollusks (squids and shellfish), arthropods (crustaceans, insects, and trilobites), and chordates, the phylum to which all vertebrates belong."
These new, fundamental body plans appeared all at once, and without the expected Darwinian intermediate forms.
In addition, we should observe in passing that there is also an underlying problem with the commonly encountered natural selection model, in which small variations confer significant cumulative advantages in populations,and cumulate to give the large changes that would constitute body-plan level macroevolution. To see this, let us excerpt a typical definition of natural selection:
Natural selection is the process by which favorable heritable traits become more common in successive generations of a population of reproducing organisms, and unfavorable heritable traits become less common. Natural selection acts on the phenotype, or the observable characteristics of an organism, such that individuals with favorable phenotypes are more likely to survive and reproduce than those with less favorable phenotypes. The phenotype's genetic basis . . . will increase in frequency over the following generations. Over time, this process can result in adaptations that specialize organisms for particular ecological niches and may eventually result in the emergence of new species. In other words, natural selection is the mechanism by which evolution may take place in a population of a specific organism. [Emphases added.]
From this, we may immediately observe that natural selection is envisioned as a probabilistic culler of competing sub-populations with varying adaptations coming from another source [usually some form of chance-based variation]. That is, it does not cause the actual variation, it is only a term that summarises differences in likelihood of survival and reproduction and possibly resulting cumulative effects on populations across time. So, when innovations in life-forms require the origin of functionally specific, information-rich organised complexity, we are back to some form of chance variation to explain it, and soon run right back into the FSCI-origination barrier.
Evolutionary layering and the limits to cellular perfection 2
Although observations from biochemistry and cell biology seemingly illustrate hundreds of examples of exquisite molecular adaptations, the fact that experimental manipulation can often result in improvements in cellular infrastructure raises the question as to what ultimately limits the level of molecular perfection achievable by natural selection. Here, it is argued that random genetic drift can impose a strong barrier to the advancement of molecular refinements by adaptive processes. Moreover, although substantial improvements in fitness may sometimes be accomplished via the emergence of novel cellular features that improve on previously established mechanisms, such advances are expected to often be transient, with overall fitness eventually returning to the level before incorporation of the genetic novelty. As a consequence of such changes, increased molecular/cellular complexity can arise by Darwinian processes, while yielding no long-term increase in adaptation and imposing increased energetic and mutational costs.