Gametogenesis

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The Histology Wizard

Күн бұрын

Пікірлер: 33

@julius1081 3 ай бұрын

This video is educational gold! Thank's from germany!

@thehistologywizard5783 3 ай бұрын

Glad you enjoyed it!

@amaka9541 3 жыл бұрын

I really love your tutorial

@thehistologywizard5783 3 жыл бұрын

Thank you, I'm glad you like them.

@thejohnringo 9 ай бұрын

Truly first rate, excellent.

@thehistologywizard5783 9 ай бұрын

Wow, thanks!

@bararich8 9 ай бұрын

Genius! Thanks a lot for this video!

@thehistologywizard5783 9 ай бұрын

You're welcome!

@daoudamer5067 Ай бұрын

Hi doctor, I study in french and the books that I went through dont say that PGC turn to spermatogonium after puberty, but they say that this phase happend before, and some argue that they turned into spermatocyte 1 and stop in the early stages of meotic devision until puberty, what do you think about this Dr.

@thehistologywizard5783 Ай бұрын

The consensus in the literature seems to be that spermatogenesis begins at puberty. This is when there is an increase in Gonadotrophin-Releasing Hormone, and thus follicle stimulating hormone and luteinizing hormones which influence Leydig cells to produce androgens. We know that that androgen surge at puberty from Leydig cells is required for spermatogenesis, since in cases where only Sertoli cells are produced, there are no spermatogenic cells present. PGC in the testes give rise/develop into spermatogonial stem cells, which divide infrequently. They give rise to cells that act more as transient amplifying population (type A spermatogonia)-these are the ones that are connected via a syncytium, then, they develop into type B spermatogonia and when they undergo the final mitotic division- that's when those 2 progeny are considered primary spermatocytes. Those then replicate their DNA (46 chromosomes, 4N) and hang out in meiotic prophase for ~3 weeks. Many of the cells we see are in this stage. Next they will complete meiosis 1... now they are secondary spermatocytes (23 chromosomes, 2N) and those very quickly undergo meiosis 2 to form the spermatids (23 chromosomes, 1N). None of my sources seem to indicated that some steps of spermatogenesis begin prior to puberty (other than arrival of PCGs) and "hold" in a way similar to oocyte development.

@grazygee3459 Жыл бұрын

It meant a world to me

@thehistologywizard5783 Жыл бұрын

I'm glad you found it helpful.

@EbubechukwuBlessing-ov7wh 2 ай бұрын

You are tge best❤ Thank you so much

@thehistologywizard5783 2 ай бұрын

You're welcome 😊

@abrikmohamed2336 2 жыл бұрын

Thanks a lot

@thehistologywizard5783 2 жыл бұрын

Most welcome

@thiagonascimento1087 Жыл бұрын

There is a huge doubt about it that I have never seem be answered (and that I reserached a lot, really a lot about it) and I think it will not be but I will ask anyway: is it possible for a mutation to occurs in someone germ cell during life time of the individual? because it is always said that germ line mutation occurs during gametogenesis or during zygote formation. But it is also said that mutation can occur in any cell, isn't it? so would be possible an acquired mutation in the cell that generate the germ cell or gamete during life time occur? or does an acquired mutation cannot occur in germ cell? and if it cannot occur, so then the cells that generate gametes are the only ones that cannot suffer mutation?

@thehistologywizard5783 Жыл бұрын

Hi Thiago, The short answer is that yes, mutations can and do occur in germ cells. There are mutations that occur in primordial germ cells for example that don't make it to the gonadal ridge; these are thought to give rise to non-gonadal tetratomas. Since those cells don't end up in the germline, you would likely call those acquired. A mutation that appears in a “viable” sperm cell or oocyte (that is, it COULD end up in a future zygote, not that it DOES because that is still a small probability, especially for a sperm cell)- would be a germline mutation. Remember though that the probability that a germ cell eneds up in future zygote is low, especially for a sperm cell because so many are made and very few fertilize an oocyte. In addition, most of the oocytes undergo atresia. The mutations that happen between the zygote and the sequestration of the oogenesis/spermatogenesis precursors ought to be considered to be somatic because they won’t be found in all cells of the body. A lot of what happens with mutations in germ cells has to do with the fact that these cells are are “privileged” in terms of DNA repair: they use mostly homologous recombination and other “error free” mechanisms of repair, very little Non-homologous end joining repair. So the error frequency between the zygote and the specification of oocytes is low. It is high in sperm cells but that’s because so many are made/so many replication cycles occur, they also are more devoted to “error free” repair. So for example you can have a germ cell tumor that is driven by mutations that I, at least, would consider to be somatic, but the distinction is more semantic than biological.

@thiagonascimento1087 Жыл бұрын

@@thehistologywizard5783 Hi The Histology Wizard! I really appreciate the answer, thank you so much! But there is still the doubt! Well, just like I said did not find any satisfactory explanation for this doubt issue, and I searched it in several scientific sources and nothing! I will reformulate my doubt: my about is about the possibility of an acquired mutation (during lifetime) somehow affect the gamete and then the offspring. The doubt is because the genetic consensus says (as far as it is know about it) that mutation during lifetime does not occur in the cells present in the gonads that create the gametes, or it means the germline cells, is not it, the germline is cells that create the gametes, is not is? And the big question never answered for me is about the reason and the mechanism behind the functioning of this. Well the gametes (eggs or sperms) came from other cells inside the gonads, is not it? and those cells you call germ line cells, is not it? The doubt is that the phenomenon behind it is very weird and does not make sense for me. I will explain why in a simple way: Well, as I said,, as far as I know, a mutation can occur in any cell. So if it happens to occur in the cells in the gonads (I think you call germline cells), that are responsible for creating the gametes (eggs or sperms), by logic, it would affect the gametes and then the offspring, is not it? So the consensus that those cells do not sufer mutation during life time does not make sense for me, can you understand my thinking logic? Because by the logic I know if suffer mutation in those cells it will affect the offspring, is not it? So again, I reassert my doubt: if a mutation happens to occur in those cells that create the gametes (and I mean again in those cells that create the gametes, not the gametes itself in their formation, but the cells in the gonads that create the gametes), it should be passed on to gametes (eggs or sperms) and then be passed on to offspring, and it would be an acquired mutation passed to offsrping, is not it? Because if it cannot occur, the only explanation I can think is that those cells present in gonads, that create the gametes (again, not the gametes itself, but the cells that create them), for some reason, cannot suffer mutation, so would it be the case? Obs: I know that the gametes (eggs or sperms) suffer mutation, but my question is about the cells present in the gonads, that create the gametes! Because by logic, if a mutation occur in those cells, then it will be an acquired mutation and will affect the gametes and so the offspring, becaming a acquired mutation! Obs2: I also know that there is a possibility of a epigenetic epimutation (not mutation) to affect those cells present in gonads, that generate the gametes, and then the gametes and then the offspring! But not a mutation! So concluding, the huge doubt is, as far as it is know by consensus of genetics knowledge, is how a mutation cannot occur in those cells that create the gametes, because if it happens, it will affect the gametes (eggs or sperms) and by logic it will affect the offspring, and would be an acquired mutation.

@thiagonascimento1087 Жыл бұрын

@@thehistologywizard5783 Who knows maybe someday I'll get a satisfactory explanation about this huge doubt, because unfortunately, until now, I did not have any satistactory explanation! But anyway thanks!

@Rim133 8 ай бұрын

@@thiagonascimento1087 im a year late but hope this helps, germ cells are the cells responsible for passing genetic information to offspring. Mutations occurring in germ cells after puberty can indeed lead to hereditary disorders in offspring. However, in terms of the individual with the mutation, it's not common for them to suddenly develop a disorder due to a mutation in their germ cells after puberty. The disorders that arise from mutations in germ cells after puberty would typically manifest in the offspring of that individual, rather than the individual themselves. This is because germ cells give rise to gametes (sperm or eggs), which carry genetic information to the next generation. So, mutations in germ cells after puberty could indeed lead to hereditary disorders in the individual's children but wouldn't directly cause illness in the individual who carries the mutation.For the individual themselves, disorders due to mutations in somatic cells (non-germline cells) could arise after puberty, but these wouldn't typically be passed on to offspring. Instead, they might result in conditions like cancer or other somatic disorders.

@amosceltic5910 4 жыл бұрын

Can you tell me what triggers gametogenesis

@thehistologywizard5783 4 жыл бұрын

Hi Amos, Gametogenesis is hormonally driven. Basically, it's held in check until, at puberty, the hypothalamus secretes gonadotropin-releasing hormone (GnRH) in a pulsatile manner, which acts on the anterior pituitary gland, stimulating it to release follicle stimulating hormone (FSH) and leutinizing hormone (LH). FSH and LH are released into the bloodstream and act only on the testes to encourage spermatogenesis within seminiferous tubules (action of FSH) and testosterone production by neighboring Leydig cells (action of LH) between the seminiferous tubules. For females, these same hormones drive oocyte and follicle development (female gametes are arrested in meiosis I and are in primoridial follicles). What causes that trigger to secrete GnRH in a pulsatile fashion? Well, I don't have a good answer, there are some pathways that seem to control GnRH, but the true control mechanism(s) aren't completely understood though.

@julius1081 3 ай бұрын

What decides which gene loci will be affected during crossing over in pachytene of prophase I, how does the chromosome "know" what areas will be engaged?

@thehistologywizard5783 3 ай бұрын

This is a great question and a question of pretty intense research. Additionally, there are two separate processes to explain. First there is pairing and second there is recombination. The exact signals aren’t known, but both are probably initiated by multiple redundant sequences along the chromosome, but what they are hasn’t been fully determined. Which is a fancy way of saying, we really don't understand how this happens.......