Oogenesis in mammals
Gametogenesis in mammals: Oogenesis
Mammalian oogenesis (egg production) differs greatly from spermatogenesis. The eggs mature through intricate coordination of hormones, paracrine factors, and tissue anatomy. Mammalian egg maturation can be seen as having four stages. First, there is the stage of proliferation. In the human embryo, the thousand or so PGCs reaching the developing ovary divide rapidly from the second to the seventh month of gestation. They generate roughly 7 million oogonia. While most of these oogonia die soon afterwards, the surviving population, under the influence of retinoic acid, enter then next step and initiate the first meiotic division. They become primary oocytes. This first meiotic division does not proceed very far, and the primary oocytes and remain in the diplotene stage of first meiotic prophase. This prolonged diplotene stage is sometimes referred to as the dictyate resting stage
This may last from 12 to 40 years. With the onset of puberty, groups of oocytes periodically resume meiosis. At that time, luteneizing hormone (LH) from the pituitary gland releases this block and permits these oocytes to resume meiotic division. They complete first meiotic division and proceed to second meiotic metaphase. This LH surge causes the oocyte to mature. The oocyte begins to synthesize the proteins that make it competent to fuse with the sperm cell and that enable the first cell divisions of the early embryo. This maturation involves the cross-talk of paracrine factors between the oocyte and its follicular cells, both of which are maturing during this phase. The follicle cells activate the translation of stored oocyte mRNA encoding proteins such as the sperm-binding proteins that will be used for fertilization and the cyclins that control embryonic cell division. After the secondary oocyte is released from the ovary, meiosis will resume only if fertilization occurs. At fertilization, calcium ions are released in the egg, and these calcium ions release the inhibitory block and allow the haploid nucleus to form.
The smaller cell becomes the first polar body, and the larger cell is referred to as the secondary oocyte. A similar unequal cytokinesis takes place during the second division of meiosis. Most of the cytoplasm is retained by the mature egg (the ovum), and a second polar body forms but receives little more than a haploid nucleus. (In humans, the first polar body usually does not divide. It undergoes apoptosis around 20 hours after the first
Oogenic meiosis
Oogenic meiosis in mammals differs from spermatogenic meiosis not only in its timing but in the placement of the metaphase plate. When the primary oocyte divides, its nuclear envelope, breaks down, and the metaphase spindle migrates to the periphery of the cell. This asymmetric cytokinesis is directed through a cytoskeletal network composed chiefly of filamentous actin that cradles the mitotic spindle and brings it to the oocyte cortex by myosin-mediated contraction. At the cortex, oocyte-specific tubulin mediates the separation of chromosomes, and mutations in this tubulin have been found to cause infertility. At telophase, one of the two daughter cells contains
hardly any cytoplasm, while the other daughter cell retains nearly the entire volume of cellular constituents meiotic division.) Thus, oogenic meiosis conserves the volume of oocyte cytoplasm in a single cell rather than splitting it equally among four progeny
Mammalian oogenesis (egg production) differs greatly from spermatogenesis. The eggs mature through an intricate coordination of hormones, paracrine factors, and tissue anatomy. Mammalian egg maturation has four stages. First, there is the stage of proliferation. In the human embryo, the thousand or so PGCs reaching the developing ovary divide rapidly from the second to the seventh month of gestation. They generate roughly 7 million oogonia.
The development of a normal ovary during foetal life is essential for the production and ovulation of a high-quality oocyte in adult life. Early in embryogenesis, the primordial germ cells (PGCs) migrate to and colonise the genital ridges. Once the PGCs reach the bipotential gonad, the absence of the sex-determining region on the Y chromosome (SRY) gene and the presence of female-specific genes ensure that the indifferent gonad takes the female pathway and an ovary forms. PGCs enter into meiosis, transform into oogonia and ultimately give rise to oocytes that are later surrounded by granulosa cells to form primordial follicles. Various genes and signals are implicated in germ and somatic cell development, leading to successful follicle formation and normal ovarian development. This review focuses on the differentiation events, cellular processes and molecular mechanisms essential for foetal ovarian development in the mice and humans. A better understanding of these early cellular and morphological events will facilitate further study into the regulation of oocyte development, manifestation of ovarian disease and basis of female infertility.
Normal ovarian development during embryogenesis is the key to fertility and reproductive success later in life. In mammals, reproductive capacity is limited by the size of the non-renewable pool of oocytes, which is established during foetal life. Follicles, the basic unit of the ovary, house the oocytes and are essential for their development and survival. In the early stages of development, follicles consist of an oocyte surrounded by somatic granulosa cells and the extracellular matrix. As the follicle grows and differentiates, theca cells are recruited; these cells are the source of the oestrogen substrate, androstenedione. Each month throughout the course of a female’s reproductive life, primordial follicles are activated to begin follicle development. This process culminates in a follicle that contains a mature fertilisable oocyte ready for release at ovulation. Disturbances in the initial steps or processes that facilitate foetal ovarian differentiation result in incomplete sexual development and may contribute to childhood and adult diseases such as gonadal dysgenesis, infertility or ovarian cancer. 1
Beginnings of the ovary
One of the earliest events in embryonic development is X chromosome inactivation, a process that occurs at the two-cell stage of the zygote and enables males and females to have equal transcript levels by genetic inactivation of one of the two X chromosomes in females. In mice, between the four- and eight-cell stage, inactivation of the paternally inherited X chromosome occurs in all female somatic cells. In the developing germ line, X inactivation is reactivated in primordial germ cells (PGCs) such that both X chromosomes are active in oogenesis. Epigenetic regulation of gene expression is an essential part of organogenesis and leads to heritable changes in gene function without inducing a change in the DNA sequence. DNA methylation or histone acetylation can affect such changes. The study of epigenetic events in the oocyte is an expanding field of research and involves studying the biology behind developmental processes such as genomic imprinting, X inactivation and transcriptional repression.
1. https://www.researchgate.net/publication/51818079_Mammalian_foetal_ovarian_development_Consequences_for_health_and_disease
Gametogenesis in mammals: Oogenesis
Mammalian oogenesis (egg production) differs greatly from spermatogenesis. The eggs mature through intricate coordination of hormones, paracrine factors, and tissue anatomy. Mammalian egg maturation can be seen as having four stages. First, there is the stage of proliferation. In the human embryo, the thousand or so PGCs reaching the developing ovary divide rapidly from the second to the seventh month of gestation. They generate roughly 7 million oogonia. While most of these oogonia die soon afterwards, the surviving population, under the influence of retinoic acid, enter then next step and initiate the first meiotic division. They become primary oocytes. This first meiotic division does not proceed very far, and the primary oocytes and remain in the diplotene stage of first meiotic prophase. This prolonged diplotene stage is sometimes referred to as the dictyate resting stage
This may last from 12 to 40 years. With the onset of puberty, groups of oocytes periodically resume meiosis. At that time, luteneizing hormone (LH) from the pituitary gland releases this block and permits these oocytes to resume meiotic division. They complete first meiotic division and proceed to second meiotic metaphase. This LH surge causes the oocyte to mature. The oocyte begins to synthesize the proteins that make it competent to fuse with the sperm cell and that enable the first cell divisions of the early embryo. This maturation involves the cross-talk of paracrine factors between the oocyte and its follicular cells, both of which are maturing during this phase. The follicle cells activate the translation of stored oocyte mRNA encoding proteins such as the sperm-binding proteins that will be used for fertilization and the cyclins that control embryonic cell division. After the secondary oocyte is released from the ovary, meiosis will resume only if fertilization occurs. At fertilization, calcium ions are released in the egg, and these calcium ions release the inhibitory block and allow the haploid nucleus to form.
The smaller cell becomes the first polar body, and the larger cell is referred to as the secondary oocyte. A similar unequal cytokinesis takes place during the second division of meiosis. Most of the cytoplasm is retained by the mature egg (the ovum), and a second polar body forms but receives little more than a haploid nucleus. (In humans, the first polar body usually does not divide. It undergoes apoptosis around 20 hours after the first
Oogenic meiosis
Oogenic meiosis in mammals differs from spermatogenic meiosis not only in its timing but in the placement of the metaphase plate. When the primary oocyte divides, its nuclear envelope, breaks down, and the metaphase spindle migrates to the periphery of the cell. This asymmetric cytokinesis is directed through a cytoskeletal network composed chiefly of filamentous actin that cradles the mitotic spindle and brings it to the oocyte cortex by myosin-mediated contraction. At the cortex, oocyte-specific tubulin mediates the separation of chromosomes, and mutations in this tubulin have been found to cause infertility. At telophase, one of the two daughter cells contains
hardly any cytoplasm, while the other daughter cell retains nearly the entire volume of cellular constituents meiotic division.) Thus, oogenic meiosis conserves the volume of oocyte cytoplasm in a single cell rather than splitting it equally among four progeny
Mammalian oogenesis (egg production) differs greatly from spermatogenesis. The eggs mature through an intricate coordination of hormones, paracrine factors, and tissue anatomy. Mammalian egg maturation has four stages. First, there is the stage of proliferation. In the human embryo, the thousand or so PGCs reaching the developing ovary divide rapidly from the second to the seventh month of gestation. They generate roughly 7 million oogonia.
The development of a normal ovary during foetal life is essential for the production and ovulation of a high-quality oocyte in adult life. Early in embryogenesis, the primordial germ cells (PGCs) migrate to and colonise the genital ridges. Once the PGCs reach the bipotential gonad, the absence of the sex-determining region on the Y chromosome (SRY) gene and the presence of female-specific genes ensure that the indifferent gonad takes the female pathway and an ovary forms. PGCs enter into meiosis, transform into oogonia and ultimately give rise to oocytes that are later surrounded by granulosa cells to form primordial follicles. Various genes and signals are implicated in germ and somatic cell development, leading to successful follicle formation and normal ovarian development. This review focuses on the differentiation events, cellular processes and molecular mechanisms essential for foetal ovarian development in the mice and humans. A better understanding of these early cellular and morphological events will facilitate further study into the regulation of oocyte development, manifestation of ovarian disease and basis of female infertility.
Normal ovarian development during embryogenesis is the key to fertility and reproductive success later in life. In mammals, reproductive capacity is limited by the size of the non-renewable pool of oocytes, which is established during foetal life. Follicles, the basic unit of the ovary, house the oocytes and are essential for their development and survival. In the early stages of development, follicles consist of an oocyte surrounded by somatic granulosa cells and the extracellular matrix. As the follicle grows and differentiates, theca cells are recruited; these cells are the source of the oestrogen substrate, androstenedione. Each month throughout the course of a female’s reproductive life, primordial follicles are activated to begin follicle development. This process culminates in a follicle that contains a mature fertilisable oocyte ready for release at ovulation. Disturbances in the initial steps or processes that facilitate foetal ovarian differentiation result in incomplete sexual development and may contribute to childhood and adult diseases such as gonadal dysgenesis, infertility or ovarian cancer. 1
Beginnings of the ovary
One of the earliest events in embryonic development is X chromosome inactivation, a process that occurs at the two-cell stage of the zygote and enables males and females to have equal transcript levels by genetic inactivation of one of the two X chromosomes in females. In mice, between the four- and eight-cell stage, inactivation of the paternally inherited X chromosome occurs in all female somatic cells. In the developing germ line, X inactivation is reactivated in primordial germ cells (PGCs) such that both X chromosomes are active in oogenesis. Epigenetic regulation of gene expression is an essential part of organogenesis and leads to heritable changes in gene function without inducing a change in the DNA sequence. DNA methylation or histone acetylation can affect such changes. The study of epigenetic events in the oocyte is an expanding field of research and involves studying the biology behind developmental processes such as genomic imprinting, X inactivation and transcriptional repression.
1. https://www.researchgate.net/publication/51818079_Mammalian_foetal_ovarian_development_Consequences_for_health_and_disease
