>That looks to be what your sources are saying too, with some discussion of residual sperm DNA in the uterus also affecting expression.
No U see above. I already looked at your sources (your second being the strongest) - only the fly one posits manipulation of the genetic material in the mature ova (I'll come to that later), but the lit review (2nd source) discusses changing the environment in which the embryo exists/will exist, which could affect which genes (aka traits) are expressed, i.e. "epigenetics." The second in particular discusses uterosomes transferring proteins and/or genetic info to the new sperm, or the prior sexual partner's sperm affecting the genetics of the *endometrial cells*, not the ova. Biochem/molecular biology is very nuanced and complicated - lots of moving parts.
Which is kinda funny from two ends - it's ridiculously complicated, so very difficult to simplify for the layperson, and also complicated enough to surprise and confound professionals. Which, again, is why I don't think this is a "jews lied" situation. Mendelian genetics was still the model (and it still works okay as a generalization) when I was in school 20ish years ago. But Dunning-Kruger kicks in often; the laypeople not knowing what they don't know, and the professionals knowing that they don't know everything, which is why I checked your sources. Hell, one of your sources even echoes the sentiment:
>"...Just as we think we have things figured out, nature throws us a curve ball and shows us how much we still have to learn," says lead author Dr Crean.
That's the fly one. They didn't observe the genomes, just the expressed traits (size), and they offered an explanation (without having examined the genome, even of the offspring let alone the female's ova) of genetic material being transferred to the female flies immature ova (a condition that doesn't apply to humans). On that note... it's hard enough to map the rat model onto the human one - the further you get from human (and flies don't even have spinal cords), the less likely it is to map onto humans. But they gave phenotypical (i.e. "traits expressed") evidence, not genotypical (i.e. genetic material) evidence.
You're right in principle - previous uncondomed sexual partners can potentially taint the woman's uterus and affect future offspring, but the mechanism is not through the ova. At least, not through any source you've given here.
It wouldn't be the internet if not for pedants. But this was my trade once upon a time.
Nope. Other way around. Go find a study that says “genetic material” isn’t impacted by spermatazoic retention and refutes chimerism and the observed phenomenon of offspring inheriting precious sexual partner physical traits.
Sure. I read all of your sources, and none said the genetic material in the ova change, and you can't (or won't) direct me to anything that says otherwise; I asked in good faith. The closest they came was that the sperm may change things in the endometrium/uterus, which is light years away (on a cellular level) from the ovaries, where the ova are housed. Nothing you posted said the ovaries, let alone the ova, are affected (fly guy's conjecture aside).
Now let me introduce you to "all of known human reproductive biology up to this point." Because I'm a nice guy, I'll even quote the passages:
https://histology.leeds.ac.uk/female/FRS_ova.php
>At completion of first meiotic division: one of the chromosome pairs is segregated to each of the daughter cells. For example, if there is an XY pairing, then one cell will receive the X, and one the Y chromosome pair.Thus when this division is completed, the resulting secondary oocyte has 'diploid' DNA, but the chromosome copies are only derived from one of the original chromosomes in the parent cell.
>A human infant ovary histology, showing the large number of oocytes occupying the ovary cortical region. Compare this with a mature ovary and note the absence of any follicle development in the infant. These early oocytes remain at the diplotene stage of the meiosis I during development from fetal life and postnatal childhood, until puberty when the lutenizing hormone (LH) surges stimulate the resumption of meiosis.
That's a video, so you'll have to just watch on your own, but they get to the point pretty quickly.
https://www.ncbi.nlm.nih.gov/books/NBK10008/
This one not only discusses the finite number of ova produced during gestation, but it also points out that other animals have widely varying strategies, which is why you can't neatly map the fruit fly model, even if it were more than conjecture, onto the human model. I recommend the full read.
And basically any biology textbook, mostly written by non-yids, will tell you the same. You're seeking to overturn roughly a century of understanding of human reproductive biology; you're going to have to bring a lot more than fruit flies and "possible endometrial sperm RNA/protein retention."
No U see above. I already looked at your sources (your second being the strongest) - only the fly one posits manipulation of the genetic material in the mature ova (I'll come to that later), but the lit review (2nd source) discusses changing the environment in which the embryo exists/will exist, which could affect which genes (aka traits) are expressed, i.e. "epigenetics." The second in particular discusses uterosomes transferring proteins and/or genetic info to the new sperm, or the prior sexual partner's sperm affecting the genetics of the *endometrial cells*, not the ova. Biochem/molecular biology is very nuanced and complicated - lots of moving parts.
Which is kinda funny from two ends - it's ridiculously complicated, so very difficult to simplify for the layperson, and also complicated enough to surprise and confound professionals. Which, again, is why I don't think this is a "jews lied" situation. Mendelian genetics was still the model (and it still works okay as a generalization) when I was in school 20ish years ago. But Dunning-Kruger kicks in often; the laypeople not knowing what they don't know, and the professionals knowing that they don't know everything, which is why I checked your sources. Hell, one of your sources even echoes the sentiment:
>"...Just as we think we have things figured out, nature throws us a curve ball and shows us how much we still have to learn," says lead author Dr Crean.
That's the fly one. They didn't observe the genomes, just the expressed traits (size), and they offered an explanation (without having examined the genome, even of the offspring let alone the female's ova) of genetic material being transferred to the female flies immature ova (a condition that doesn't apply to humans). On that note... it's hard enough to map the rat model onto the human one - the further you get from human (and flies don't even have spinal cords), the less likely it is to map onto humans. But they gave phenotypical (i.e. "traits expressed") evidence, not genotypical (i.e. genetic material) evidence.
You're right in principle - previous uncondomed sexual partners can potentially taint the woman's uterus and affect future offspring, but the mechanism is not through the ova. At least, not through any source you've given here.
It wouldn't be the internet if not for pedants. But this was my trade once upon a time.
I’ll wait.
Now let me introduce you to "all of known human reproductive biology up to this point." Because I'm a nice guy, I'll even quote the passages:
https://histology.leeds.ac.uk/female/FRS_ova.php
>At completion of first meiotic division: one of the chromosome pairs is segregated to each of the daughter cells. For example, if there is an XY pairing, then one cell will receive the X, and one the Y chromosome pair.Thus when this division is completed, the resulting secondary oocyte has 'diploid' DNA, but the chromosome copies are only derived from one of the original chromosomes in the parent cell.
https://open.lib.umn.edu/humanbiology/chapter/5-2-meiosis/
> At the time of birth, all future oocytes are in the prophase stage; no additional oocytes or precursors are produced after birth.
https://embryology.med.unsw.edu.au/embryology/index.php/Oocyte_Development#Oogenesis
>A human infant ovary histology, showing the large number of oocytes occupying the ovary cortical region. Compare this with a mature ovary and note the absence of any follicle development in the infant. These early oocytes remain at the diplotene stage of the meiosis I during development from fetal life and postnatal childhood, until puberty when the lutenizing hormone (LH) surges stimulate the resumption of meiosis.
https://www.khanacademy.org/science/how-does-the-human-body-work-class-12/x7babbc170453fdb8:human-reproduction/x7babbc170453fdb8:gametogenesis/v/basics-of-egg-development
That's a video, so you'll have to just watch on your own, but they get to the point pretty quickly.
https://www.ncbi.nlm.nih.gov/books/NBK10008/
This one not only discusses the finite number of ova produced during gestation, but it also points out that other animals have widely varying strategies, which is why you can't neatly map the fruit fly model, even if it were more than conjecture, onto the human model. I recommend the full read.
https://pressbooks.gvsu.edu/humangenetics/chapter/chapter-13-developmental-genetics/
And basically any biology textbook, mostly written by non-yids, will tell you the same. You're seeking to overturn roughly a century of understanding of human reproductive biology; you're going to have to bring a lot more than fruit flies and "possible endometrial sperm RNA/protein retention."