EXPLORING THE ROLE OF THE PROTEASOME ACTIVATOR PA200 IN DECREASED FERTILITY OF HD TRANSGENIC MALE MICE

Abstract

This thesis investigates the molecular mechanisms of reduced male fertility in a transgenic mouse model of Huntington’s disease (HD). The study focuses on the role of the proteasome activator PA200, which is important for normal spermatogenesis and protein degradation processes in the testes. HD and wild-type mice testes were investigated at the histological and molecular level. The results show testicular development impairment, impaired spermatogenesis, and alterations in gene expression in HD mice. These findings suggest that PA200-related proteasome activity may contribute to fertility problems in HD male mice.