Global changes in epigenomes during mouse spermatogenesis: possible relation to germ cell apoptosis

• Published in: Histochemistry and cell biology 2020-08, Vol.154 (2), p.123-134
• Main Authors: Koji, Takehiko, Shibata, Yasuaki
• Format: Article
• Language: English
• Subjects: Animals; Apoptosis; Apoptosis - genetics; Bcl-2 protein; Biochemistry; Biomedical and Life Sciences; Biomedicine; Cell Biology; Chromatin - chemistry; Chromatin - genetics; Chromatin - metabolism; Chromatin remodeling; Developmental Biology; Endocrine disruptors; Environmental factors; Epigenetics; Epigenome - genetics; FasL protein; Gene expression; Genomes; Germ cells; Germ Cells - metabolism; Germ Cells - pathology; Mammals; Mice; Mitochondria; Molecular modelling; Review; Spermatogenesis; Spermatogenesis - genetics
• ISSN: 0948-6143; 1432-119X
• DOI: 10.1007/s00418-020-01900-x

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.