Aberrant sperm morphology hinders sperm motility and causes male subfertility. Spermatogenesis, a complex process in male germ cell development, necessitates precise regulation of numerous developmental genes. However, the regulatory pathways involved in this process remain partially understood. We have observed the widespread expression of , the gene encoding a nucleosome-destabilizing factor, in mouse testicular cells. Our study demonstrates that mice experiencing depletion in spermatogenic cells exhibit subfertility characterized by a diminished count and motility of spermatozoa. Furthermore, the rate of sperm malformation significantly increases in the absence of , with a predominant occurrence of head and neck malformation in spermatozoa within the cauda epididymis. Additionally, a reduction in spermatocyte numbers across different meiotic stages is observed, accompanied by diminished histone acetylation in spermatogenic cells upon depletion. Our findings underscore the crucial roles of in mouse spermiogenesis and unveil novel insights into the etiology of male reproductive diseases.

中文翻译：

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核小体不稳定因子 GLYR1 的缺乏会抑制小鼠的精子发生

精子形态异常会阻碍精子活力并导致男性生育力低下。精子发生是男性生殖细胞发育中的一个复杂过程，需要对众多发育基因进行精确调控。然而，这一过程中涉及的监管途径仍部分被了解。我们观察到编码核小体不稳定因子的基因在小鼠睾丸细胞中广泛表达。我们的研究表明，生精细胞耗竭的小鼠表现出生育能力低下，其特征是精子数量和活力减少。此外，在缺乏 的情况下，精子畸形率显着增加，附睾尾内的精子主要发生头颈畸形。此外，观察到不同减数分裂阶段精母细胞数量的减少，伴随着生精细胞中组蛋白乙酰化的减少。我们的研究结果强调了小鼠精子发生中的关键作用，并揭示了对男性生殖疾病病因学的新见解。