Can Two Y Genes Replace the Y Chromosome in Mice?


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Can Two Y Genes Replace the Y chromosome in Mice?
The Y chromosome is important in any kind of reproduction because it determines if you’re going to be a male or female. The article claims that live mouse descendants can be created using germ cells from males with the Y chromosome to two genes. The SRY gene is called the sex determining region because it has instructions to make a transcription factor and develops as a male.
The Y chromosome gene is required to drive mouse sperm cells to cause mitosis in a cell allowing formation of haploid germ cells assisted in reproduction. The Y chromosome in animals are unused, scientists are thinking that they are involved in male reproduction. They investigated to see which genes are important for keeping sperm functions. They were able to do this by using ART they can take out several steps of normal human fertilization using attached, nonviable, immature sperm. They tested to see if infertile male mice lack the Y chromosome long arm and generate live offspring. When the structure of abnormal sperm are delivered in an immature egg cell in the ovary by a vitro fertilization procedure where a sperm is injected into an egg. The Y chromosome inside the mouse is reduced from 78 Mb to about 2 Mb and encodes seven genes and three gene families.
Animal testes are determined by the SRY and signals gonads to make differentiation. On the occasion with the addition of SRY, mice with one chromosome develop testis that are inhabited in any cells in the gonads. The cells have potential to increase in cell number by division and meiotic and post meiotic stages of spermatogenesis when they are not present. When scientists found an organism that was missing the Y gene, it gave rise to the idea that Eif2s3y was a gene that restored the ability to make sperm and spread it. In the X chromosome the males transgenic for Ei2s3y , the gonads showed to finish the meiotic prophase and the first meiotic division before the secondary spermatocytes. The scientists tested if the spermatid cells from the secondary spermatid cells were useful in ART and if other components of the Y chromosome increase in order to make functional gametes.
They observed if the mice with the Y gene was autosomally located in SRY and if the X chromosome was located in Eif2s3y. The mice had testes that are smaller than wild type XY in males but are populated with germ cells.

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When the testicle sections proved that the induction of mitosis in a cell was ongoing, it allowed the development of germ cells with spermatid form like the ones seen earlier. The visibility of the spermatid were low and the advancement was restricted to steps five to seven, occasionally the presence of steps eight to nine were visible. They were able to see secondary changes to the tubules with the formation of ‘nucleic bodies’, vacuoles, and dying germ cells. This increased for males as they aged and led to a male disorder by syndrome tubules.
They tested the function of spermatid cells from X^EOSry in ART. They found an increased size and the surface was rough not smooth when compared to the spermatid in XY males. When they performed the spermatid injection, the mice were able to father their offspring. This was possible because of the pair of pronuclei and the ability to make the second polar body and the cleavage. When the embryos were moved to the oviducts of the females, the offspring were kept. 3 out of 4 mice were that had the injection of the spermatids had fathered an offspring. the mice that used ROSI with E^EOSry were lower than XY controls. The progeny had the expected genotypes as expected from the X^EOSry fathers. A sex chromosome that hasn’t been paired can lead to apoptosis or meiotic arrest. The spermatids that were found in the testis could be the ones that were ‘leaked’ through meiotic arrest.
Figure 1 shows male Eif2s3y and SRY, they have meiotic and post meiotic arrests and sometimes forming spermatids that delay and don’t develop stages eight to nine.1B shows a dying tubule with the formation of multinucleate bodies.1C shows the tubule syndrome in an old male.1D shows testicular suspension of the normal type of male that has testicular sperm and spermatids. 1F shows the ROSI baby after the transfer of embryos with spermatids from a male with two Y genes. 1G shows a female that came from the baby shown in 1F with her liter.
Table one show the results of spermatid injection using ROSI with male spermatid that have a limited Y gene. The percentages of the offspring and the implants were found by the transferring of the embryos. In figure 2 there is a bar graph and the X axis is labeled ‘percent of haploid spermatid’ and the Y axis is ‘age in days.’ The male genotypes are X^ESOry, X^EY*Sry, X^ESXR^bO, X^ESxr^by*x and XY^III control. Every bar represents one male that has testicular cells, the percentage above the bar is the number of babies after ROSI. The percentage in boxes in the blue color is the average percentage of haploid spermatids. The percentage in the red color is the babies’ genotype using ROSI. The male control genotype is 97% of the haploid spermatid. The males with X^ESxr^bY*^x had a higher average of haploid spermatid than the other genotypes.
The spermatid DNA and the zygote chromosome results showed that most of the spermatids from male X^EOSry were diploid and stopped the triploid zygotes. If they wanted to change this, they can use the males in Y*^x in order to have a second pairing location. In the male X^EY*xSry the pairing was 85% successful in the Y*x and X. The testicular phenotype didn’t change and the proportion of the living offspring after injection was low. They tested to see ploidy and showed that most of the X^EY*xSry spermatids are diploid and that the spermatids using ROSI are triploid. Meaning that the X chromosome has the same relevance as X^EY*xSry in males were not affected in meiotic arrest and boosting up the ROSI efficiency.
They wondered if other Y chromosome genes are good for spermatid functions in ART, they used males where the SRY transgene driving was taken changed to a sex reverse factor. In the males X chromosome carries Eif2s3y needed for spermatagonial proliferation and with the Sxr^b. Male testis that came from X^ESxr^bO and X^ESxr^bY*x were not only bigger than X^EOSry and X^EY*Sry but also smaller than XY in males. The spermatids appeared more in X^ESxr^bY*x, in both males the spermatid was more advanced because they had clear elongation all the way to step 10, sometimes up to step 11 or 12. The secondary changes in X^ESxr^bY*x in males was less than other genotypes. The zygote chromosome proved that most zygotes after ROSI were diploid and the outcome of ROSI improved with all the males they tested on. The male frequency in X^ESxr^bO of haploid spermatids stayed low. The difference between ploidy of spermatids and zygotes gave idea to a second meiotic division could have happened in the oocytes.




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