个人陈述：调节基因表达的DNA甲基化
它本质上是说DNA甲基化aion的水平在每个生殖系细胞发育过程中都会发生变化。在本研究中，我们观察到人类生殖系细胞的DNA甲基化，表明在PGC t6wga的迁移过程中可以检测到5mC。这是发现，有定性变化的每一种免疫细胞化学方法使用。在迁移后的胚胎生殖细胞中，5mc -阴性。这在人类睾丸和卵巢中也被发现。男性胎儿睾丸生殖细胞在18wga左右重获5mC;只有在出生后才发现5mC。结果表明，与6wga时的体细胞相比，5mC有明显的质性降低。从这一点，它指出了一个事实，DNA低甲基化和PGCs开始失去5mC通过生殖细胞生化途径。DNA甲基化与多功能基因的抑制有关。在这种情况下，研究表明6wga是低甲基化的，这可能是由于多潜能基因的激活。
在这项研究中，只有一个样本被用来了解组织的可用性。需要更多的样本才能得出全球5mC水平正在迁移人类PGC的结论。在小鼠的情况下，DNA去甲基化已被发现调节迁移后生殖细胞的温和表达。然而，这在迁移后的人类特征生殖细胞中很难检测到。这与之前的研究结果相关，也提示成熟生殖细胞特异性基因表达上调。人类DNA甲基化研究表明，在一些晚期胎儿睾丸生殖细胞中重新检测到5mC，但在所有检测到的妊娠期，胎儿卵巢生殖细胞中仍然检测不到5mC。因此，人类卵巢生殖细胞DNA从头甲基化的延迟与人类胚胎卵巢中DAZL的进一步上调和减数分裂基因的激活有关。为了进一步了解5mC和5hmC改性的细微差别，本文对其进行了详细的分析。研究中发现5C染色于。
以往的研究表明，生殖细胞中5mC和5hmC的存在会影响人类生殖细胞(Dawlaty et al.， 2011)。这表明它们并没有参与甲基化过程，而是参与了生殖细胞的表观遗传控制。从8 ~ 18wga的6wga中，几乎所有迁移后的雄性和雌性生殖细胞均为5mc阴性。男性胎儿睾丸生殖细胞在18wga左右重新检测到5mC;在女性中，5mC在出生后的人类卵巢生殖细胞中恢复。5hmC和5Mc的确切函数尚不清楚。对于这种5mC到5hmC TET I蛋白的转化起主要作用。在研究过程中发现，粉防己碱1、2和3蛋白在妊娠初期的水平较高。妊娠进程影响了它们的表达方式。他们被发现在这段时间内处于较低的水平。在该粉防己碱中发现了各阶段的蛋白。发现粉防己碱1和粉防己碱3蛋白在妊娠三个月期间存在差异。有必要探讨确定其确切功能的确切机制。
个人陈述 ：调节基因表达的DNA甲基化
It essentially states that the levels of DNA methylaion changes during each of germ line cells development. In this research it has been observed that DNA methylation in human germ line cells showcased that 5mC was detectable during the migration PGC t 6wga. This was found that there was qualitative variation for each immunocytochemistry method that was used. In the post migratory fetal germ cell the 5mC-negative. This was found again in the asynchronously in human testis and ovary. In the male, 5mC was regained in human fetal testicular germ cell at around 18wga in the case of women; it was 5mC was found only after the birth. It was found that the qualitative reduction of the 5mC when compared with the somatic cells at 6wga. From this it points towards the fact that DNA hypomethylation and that PGCs starts to lose 5mC to adopt the germ cell biochemical pathways. DNA methylation has been associated with the repression of the pluripotent gene. In this case the research indicated that the 6wga was hypomethylated, this could be due to the activation of the pluripotency gene.
IN this research there was only one sample that was used to understand about the availability of the tissue. There are more samples that are required to come to a conclusion that the global level of 5mC is migrating human PGC. In the case of mice DNA demethylation has been found to regulate the temperate expression of the post migratory germ cell. This was however difficult to detected in post migratory human featl germ cell. This is associated with the previous findings that also suggest that the up regulation of the mature germ cell-specific gene expression. The DNA methylation studies in human here showed that 5mC was redetected in some of the later fetal testicular germ cells, but remained undetectable in the fetal ovarian germ cells across all the detected gestations. Thus, the delay of DNA de novo methylation in human ovarian germ cells correlates with further upregulation of DAZL and the activation of meiotic genes in human fetal ovary. To further understand the nuances of the situation 5mC and 5hmC modification has been probed in detail in this analysis. It has been found in the research that 5C staining at.
Previous studies and research indicates that the human germ cell is influenced by the presence of 5mC and 5hmC in germ cells (Dawlaty et al., 2011). This suggests that rather than being involved in the methylation process they are involved in the epigenetic control of the germ cells. 6wga from 8-18wga, nearly all of the postmigratory male and female germ cells were 5mC-negative. In male, 5mC was redetected in human fetal testicular germ cell at around 18wga; in female, 5mC was regained in human ovarian germ cells after birth. Exact function is yet to be known of the 5hmC and 5Mc. For this conversion of 5mC to 5hmC TET I proteins play a major role. During research it was found that the TET 1, 2 and 3 proteins were found in higher levels during the initial 1st trimester stage. Progression of the gestation impacted how they were expressed. They were found to be in reduced levels during these times. In this TET 2 protein was found in all stages. TET 1 and 3 proteins were found to vary across the trimesters. There is need to probe into the exact mechanisms to identify their exact functions.
