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Mol Cell Endocrinol ; 586: 112194, 2024 May 15.
Article in English | MEDLINE | ID: mdl-38395189

ABSTRACT

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 Glyr1, the gene encoding a nucleosome-destabilizing factor, in mouse testicular cells. Our study demonstrates that mice experiencing Glyr1 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 Glyr1, 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 Glyr1 depletion. Our findings underscore the crucial roles of Glyr1 in mouse spermiogenesis and unveil novel insights into the etiology of male reproductive diseases.


Subject(s)
Nuclear Proteins , Nucleosomes , Oxidoreductases , Sperm Motility , Spermatogenesis , Animals , Male , Mice , Nucleosomes/metabolism , Semen , Sperm Motility/genetics , Spermatogenesis/genetics , Spermatozoa/metabolism , Testis/metabolism , Nuclear Proteins/genetics , Oxidoreductases/genetics
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