Establishment of recovery spermatogenesis after chemotherapy due to the microenvironment modulation in seminiferous tubule

从NCBI中检索遗传信息的结果，选择了因各种抗癌药物而选择性受损的基因。此外，使用抗癌药物治疗后的恢复相关蛋白也与减数分裂阶段表达的基因相关。这些候选基因有助于精子发生，并且对各种抗癌药物的作用取决于它们的剂量。一般来说，减数分裂阶段最重要的过程是同源染色体的准确分布。据推测，染色体间的同源重组最初发生在减数分裂初期的瞬时DNA双链断裂（DSB）中。在同源链的交叉反应中，Rad51或Rad52、Rad54、Rad55、Rad57、DMC1、Rpa1等蛋白在真核生物中起核心作用。特别是，据报道，根据敲除小鼠，RAD51在减数分裂阶段没有取代DMC1 （GenBank, NM_007068）的功能。DMC1的转录本在减数分裂阶段具有特异性，并且只能识别同质链。我们的研究表明，DMC1转录本存在三种选择性剪接产物。临床上这些转录本在特发性男性不育症中有不同数量。通过对临床样本的分析，我们认为这些同工异构体的数量导致了DMC1的一个基序和结构域的修饰，并可能诱导精子细胞凋亡。这些基因剪接变异对减数分裂的控制起着重要作用，并对精子发生的可能性产生影响。我们的研究表明，精子发生阻滞的一种机制与减数分裂早期的功能障碍有关，这是由结构域特异性蛋白衍生的异构体引起的。

As a result of having retrieving genetic information from NCBI, a gene which was damaged selectively due to the various anti-cancer agents has been selected. Moreover recovery-related proteins after treating using anti-cancer agents were also associated with the genes during expressing in the meiotic stage. These candidate genes contributed to spermatogenesis and were naive to various anti-cancer agents depended on their dose. Generally speaking, the most important process of meiotic stage is accurate distribution of homologous chromosomes. It is assumed that the homologous recombination between chromosomes occurred initially in a transient DNA double-strand break (DSB) in the beginning to meiotic stage. In the cross reaction between homologous strands, the proteins such as Rad51 or Rad52, Rad54, Rad55, Rad57, DMC1, Rpa1 play a central role in a eukaryote. Specially, it is reported that RAD51 has not replaced the function of DMC1 (GenBank, NM_007068) in meiotic stage according to the knockout mouse. The transcripts of DMC1 are particularly specific in meiotic stage and enable to recognize only homogenous strands.Our study revealed that the transcripts of DMC1 were existed three products derived from alternative splicing. Clinically these transcripts had a various number in the idiopathic male infertility. According to analyzing the clinical samples, it was suggested that the number of the isoforms leaded to modify a motif and domain of the DMC1, and was thought to be induced apoptosis of spermatid. These genetic splicing variants contributed to meiotic control and clarified to affect the possibility of the spermatogenesis. Our study showed that one mechanism of spermatogenesis arrests was associated with the dysfunction of early stage during meiosis due to isofoms derived from domain specific proteins.