DNA double-strand break repair in male germ cells during spermatogenesis and its association with male infertility development

IF 3 3区生物学 Q2 GENETICS & HEREDITY DNA Repair Pub Date : 2022-10-01 DOI:10.1016/j.dnarep.2022.103386

Gunel Talibova, Yesim Bilmez, Saffet Ozturk

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引用次数: 3

Abstract

Spermatogenesis is a complex developmental process. During this process, male germ cells from spermatogonia to sperm cells encounter a number of DNA damages. The most severe form of these damages is double-strand breaks (DSBs) deriving from exogenous and endogenous genotoxic insults. DSBs must be correctly repaired in a short time to maintain genomic integrity in the male germ cells. For this purpose, there are four pathways working in repair of DSBs: homologous recombination (HR), classical non-homologous end joining (cNHEJ), alternative end joining (aEJ), and single strand annealing (SSA). While the HR pathway repairs DSBs with a homology-based and error-free manner, the cNHEJ, aEJ, and SSA pathways join free ends in a sequence-independent mechanism. Possible impairments in these DSB repair mechanisms can lead to cell cycle arrest, abnormal meiotic recombination, and ultimately male infertility. In this review, we comprehensively introduce DSB repair pathways being used by male germ cells during spermatogenesis. Also, potential relationship between dysfunction in these pathways and male infertility development are discussed in the light of existing studies.

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精子发生过程中男性生殖细胞DNA双链断裂修复及其与男性不育发展的关系

精子发生是一个复杂的发育过程。在这个过程中，男性生殖细胞从精原细胞到精细胞会遇到一些DNA损伤。这些损伤最严重的形式是由外源性和内源性基因毒性损伤引起的双链断裂(DSBs)。必须在短时间内对dsb进行正确修复，以保持雄性生殖细胞基因组的完整性。为此，dsb的修复有四种途径:同源重组(HR)、经典非同源末端连接(cNHEJ)、替代末端连接(aEJ)和单链退火(SSA)。HR通路以基于同源性和无错误的方式修复dsb，而cNHEJ、aEJ和SSA通路以序列无关的机制连接自由端。这些DSB修复机制的损伤可能导致细胞周期停滞，减数分裂重组异常，最终导致男性不育。本文将全面介绍DSB修复途径在精子发生过程中被用于男性生殖细胞。同时，结合已有研究，讨论了这些通路功能障碍与男性不育症发展的潜在关系。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

DNA Repair 生物-毒理学

CiteScore

7.60

自引率

5.30%

发文量

审稿时长

59 days

期刊介绍： DNA Repair provides a forum for the comprehensive coverage of DNA repair and cellular responses to DNA damage. The journal publishes original observations on genetic, cellular, biochemical, structural and molecular aspects of DNA repair, mutagenesis, cell cycle regulation, apoptosis and other biological responses in cells exposed to genomic insult, as well as their relationship to human disease. DNA Repair publishes full-length research articles, brief reports on research, and reviews. The journal welcomes articles describing databases, methods and new technologies supporting research on DNA repair and responses to DNA damage. Letters to the Editor, hot topics and classics in DNA repair, historical reflections, book reviews and meeting reports also will be considered for publication.