What factors influence gametogenesis?

Question

(This is not homework...)
I think it's probably hormones, temperature, drugs, etc. But I don't know the details. Can anybody help me?

Answer 1

Major factors that influence gametogenesis include hormones, or rather, the coordination of different hormones in the body, especially the sex hormones.

In males, testosterone is the key sex hormone. It is primarily for gametogenesis (sperm) and works hand-in-hand with the androgen binding factor (ABF), which is responsible for concentrating testosterone to where the sperm are produced, thereby nourishing them for development. There is also the follicle-stimulating hormone, which can also initiate spermatogenesis. Temperature plays a very major role in spermatogenesis. Sperm cannot be produced at body temperature. This is why males have a scrotum so that the testes could lie outside the main body by descending outward onto the pouch-like structure (the scrotum). Dietary deficiencies (such as vitamins B, E and A), anabolic steroids, metals (cadmium and lead), x-ray exposure, dioxin, alcohol, and infectious diseases will also adversely affect the rate of spermatogenesis.

In females, the coordination of the different sex hormones also play a major role in gametogenesis. Follicle-Stimulating Hormone (FSH) instructs the follicle cells in the ovaries to produce estrogen, which in turn nourishes the developing oocyte to undergo meiosis, among many other things. When the oocyte is mature enough to be released from the ovary into the oviduct (process called ovulation), signals are sent to the brain to produce Luteinizing Hormone (LH), which instructs the ovary to convert the remaining follicle into what is called a corpus luteum. LH also instructs the same cells that produced estrogen before ovulation to now produce progesterone.

Answer 2

I'm not entirely sure what you are looking for. Obviously, the biggest influence is your sex. Males go through spermogenisis and females ogogenisis. Males produce gametes throughout their lifetime, and are more susceptible to environmental influences such as pollution. Females produce oocytes before birth, which ripen (undergoes meiosis to become ovum) during their cycle. Each can be influenced by the environment - i.e. hormones, drugs, temperature, ect., but the exact influence will vary.

Answer 3

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Answer 4

Reproduction and ageing : Most discussion of the evolution of ageing focuses on its effects on mortality, rather than reproduction, in spite of the fact that in terms of an impact on fitness, the form of the reproductive schedule is as important as that of the mortality curve. A good reason for this is that many aspects of reproductive senescence can be explained in the same general terms as physiological senescence. Nevertheless, in addition to the important issues of the trade-offs between survival and fecundity, considered earlier, there are intriguing evolutionary questions about the links between reproduction and ageing, notably the significance of post-reproductive survival (where it occurs) and the effects of damage and selection on the germ line.
The existence of a distinct post-reproductive phase is characteristic of certain semelparous species, in which individuals reproduce only once. On the other hand, many semelparous species undergo extremely rapid senescence on completion of reproduction, often as a direct consequence of the massive physiological changes associated with an explosive reproductive burst5. The evolutionary basis of semelparity is well understood, and from the perspective of the evolutionary theories of ageing, semelparity represents an extreme version of the decline in the force of natural selection with age. In a semelparous species, the force of natural selection approximates a step function, being uniformly high until reproduction begins, and declining abruptly as reproduction is completed, because the chance of surviving to breed again is effectively zero. This explains the sudden collapse of any pressure to invest in somatic maintenance and repair. Whether or not there is significant post-reproductive survival may be governed chiefly by whether or not the post-reproductive adult contributes actively to the survival chances of the offspring.


A very different example of post-reproductive survival is the human menopause, where fertility in iteroparous human females comes to a relatively abrupt halt at around the age of 45–50 years, when the impact of senescence on most other functions is still small. Although the proximate cause of menopause seems to be oocyte depletion (linked also with neuroendocrine changes), this begs the question why natural selection has not produced a store of oocytes which lasts for longer. One possibility is that during most of humanity's evolutionary history, women rarely survived beyond 45–50 years, so selection simply produced about as many oocytes as would be required. But evidence from hunter–gatherer communities indicates that even though average life expectancy is short, women who avoid the hazards of early life and reach childbearing age have a reasonable chance of surviving to the age of menopause and beyond. This indicates that the menopause may have a deeper evolutionary significance.


Early female reproductive senescence has been reported in other species (for example, chimpanzees, macaques and toothed whales) but is generally less clear-cut, indicating that if the menopause has an evolutionary basis, this may be found in the special circumstances of the human life history. In particular, menopause could be linked with the evolution of human longevity, notably, through the effects of increased brain size and sociality. Increased neonatal brain size coupled with the constraint on the birth canal imposed by the mechanics of a bipedal gait has made giving birth unusually difficult for human females. The risks of childbearing, particularly in the absence of modern obstetric care, would increase even more steeply with age if fertility were to persist during the later period of the life span. The problem of a large brain size is also reflected in the fact that human infants are born unusually early, relative to other species, with respect to the completion of brain growth and development. Infants remain highly dependent for extended periods and, in the ancestral environment, their survival will have been unlikely if their mother died in childbirth. There may thus be a fitness advantage in limiting reproduction to ages when it is comparatively safe, thereby increasing the likelihood of the mother surviving to raise her existing offspring to independence. In addition, post-menopausal women may contribute to the successful rearing of their grandchildren, by providing assistance to their own adult offspring and thereby increasing their inclusive fitness, that is, their overall genetic contribution to future generations. It is likely that a combination of all of these factors is required to explain the human menopause, which may account for the lack of evolutionary support for menopause in other species.


Human reproductive ageing also highlights the interesting puzzle that although the germ line must, in a fundamental sense, be immortal (as damage cannot be permitted to accumulate across generations without immediate risk of extinction), there is clear evidence that individual germ cells do accumulate faults. Indeed, it would be surprising if the germ line was immune to accumulation of damage, because germ cells are subject to the same kinds of molecular damage as somatic cells. From a statistical perspective it is clear that the germ-cell population does undergo significant ageing. In the case of the human ovary the rate of follicular loss accelerates from around age 35 years, and male fertility begins to decline from around age 30. There is also an increase in the frequency of chromosomal abnormalities in newborn children as a function of maternal and, to a lesser extent, paternal age. Nevertheless, healthy children born to older parents are not prematurely aged, although there is some suggestion that daughters' (but not sons') longevity is adversely affected by advanced paternal age. Thus, either germ cells are endowed with special maintenance and repair systems the enzyme telomerase being a good example or selection at the cell or embryo level during gametogenesis, conception and pregnancy serves to screen out most faults. It may be relevant that during each human menstrual cycle about 20 ovarian follicles are triggered to start the process of maturation, although usually only one completes its development and is ovulated. A mechanism of probable significance in the evolution of female germ-line immortality is the stringent bottleneck in the size of the cellular mitochondrial population in early embryogenesis. A healthy complement of mitochondria is essential for subsequent viability of the offspring, and mutations in mitochondrial DNA (mtDNA) tend to accumulate with age. If the mitochondrial population in the oocyte contains a fraction of organelles bearing mtDNA mutations, a bottleneck coupled with an effective quality screen might select embryos that carry only intact mitochondria.