SIN-3 acts in distinct complexes to regulate the germline transcriptional program in Caenorhabditis elegans.

ABSTRACT: The transcriptional co-regulator SIN3 influences gene expression through multiple interactions that include histone deacetylases. Haploinsufficiency and mutations in SIN3 are the underlying cause of Witteveen-Kolk syndrome and related intellectual disability and autism syndromes, emphasizing its key role in development. However, little is known about the diversity of its interactions and functions in developmental processes. Here, we show that loss of SIN-3, the single SIN3 homolog in Caenorhabditis elegans, results in maternal-effect sterility associated with de-regulation of the germline transcriptome, including de-silencing of X-linked genes. We identify at least two distinct SIN3 complexes containing specific histone deacetylases and show that they differentially contribute to fertilit

SUBMITTER: Robert VJ 

PROVIDER: S-EPMC10617626 | biostudies-literature | 2023 Nov

REPOSITORIES: biostudies-literature