AI Article Synopsis
- HP1β, encoded by the Cbx1 gene, is essential for chromatin condensation, transcription regulation, and DNA damage repair.
- Conditional knockout of Cbx1 in mouse testes disrupts male germ cell development, impacting sperm maturation and causing seminiferous tubule degeneration.
- The absence of HP1β is linked to increased DNA damage, evidenced by elevated γ-H2AX foci, indicating that HP1β loss leads to replication defects and affects spermatogenesis.
Article Abstract
Heterochromatin protein 1β (HP1β), encoded by the Cbx1 gene, has been functionally linked to chromatin condensation, transcriptional regulation, and DNA damage repair. Here we report that testis-specific Cbx1 conditional knockout (Cbx1 cKO) impairs male germ cell development in mice. Depletion of HP1β negatively affected sperm maturation and increased seminiferous tubule degeneration in Cbx1 cKO mice. In addition, the spermatogonia have elevated γ-H2AX foci levels as do Cbx1 deficient mouse embryonic fibroblasts (MEFs) as compared to wild-type (WT) control MEFs. The increase in γ-H2AX foci in proliferating Cbx1 cKO cells indicates defective replication-dependent DNA damage repair. Depletion or loss of HP1β from human cells and MEFs increased DNA replication fork stalling and firing of new origins of replication, indicating defective DNA synthesis. Taken together, these results suggest that loss of HP1β in proliferating cells leads to DNA replication defects with associated DNA damage that impact spermatogenesis.
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| http://dx.doi.org/10.1007/s00412-020-00739-4 | DOI Listing |
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