Mammalian spermatogenesis is characterized by disproportionate germ cell apoptosis. The high frequency of apoptosis is considered a safety mechanism that serves to avoid unfavorable transmission of paternal aberrant genetic information to the offspring as well as elimination mechanism for removal of overproduced immature or damaged spermatogenic cells. The molecular mechanisms involved in the induction of germ cell apoptosis include both intrinsic mitochondrial Bcl-2/Bax and extrinsic Fas/FasL pathways. However, little is known about the nuclear trigger of those systems. Recent studies indicate that epigenomes are essential in the regulation of gene expression through remodeling of the chromatin structure, and are genome-like transmission materials that reflect the effects of various environmental factors. In spermatogenesis, epigenetic errors can act as the trigger for elimination of germ cells with abnormal chromatin structure, abnormal gene expression and/or morphological defects (disordered differentiation). In this review, we focus on the relationship between global changes in epigenetic parameters and germ cell apoptosis in mice and other mammals.

哺乳动物的精子发生特征是生殖细胞凋亡不成比例。高频率的细胞凋亡被认为是一种安全机制，可避免父系异常遗传信息向后代的不利传播，以及消除过量产生的未成熟或受损的生精细胞的消除机制。诱导生殖细胞凋亡的分子机制包括内在的线粒体Bcl-2 / Bax和外在的Fas / FasL途径。但是，对于这些系统的核触发机制知之甚少。最近的研究表明，表观基因组通过染色质结构的重构在基因表达的调控中至关重要，并且是反映各种环境因素影响的类似基因组的传播材料。在生精中 表观遗传错误可以作为消除具有异常染色质结构，异常基因表达和/或形态缺陷（无序分化）的生殖细胞的诱因。在这篇综述中，我们关注小鼠和其他哺乳动物表观遗传参数的全局变化与生殖细胞凋亡之间的关系。