Fance deficiency impaired DNA damage repair of prospermatogonia and altered the repair dynamics of spermatocytes.

ABSTRACT:

Background

Non-obstructive azoospermia (NOA) is the most severe form of male infertility and affects approximately 1% of men worldwide. Fanconi anemia (FA) genes were known for their essential role in DNA repair and growing evidence showed the crucial role of FA pathway in NOA. However, the underlying mechanisms for Fance deficiency lead to a serious deficit and delayed maturation of male germ cells remain unclear.

Methods

We used Fance deficiency mouse model for experiments, and collected testes or epididymides from mice at 8 weeks (8W), 17.5 days post coitum (dpc), and postnatal 11 (P11) to P23. The mice referred to three genotypes: wildtype (Fance ^+/+), heterozygous (Fance ^+/-), and homozygous (Fance ^-/-). Hematoxylin and eosin staining, i

SUBMITTER: Yin H 

PROVIDER: S-EPMC11360510 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature