SIN3 acts in distinct complexes to regulate the germline transcriptional program in C. elegans [sin-3(tm1276)]
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ABSTRACT: The SIN3 transcriptional coregulator influences gene expression through multiple interactions that include histone deacetylases (HDACs). Haploinsufficiency and mutations in SIN3 are the underlying cause of Witteveen-Kolk syndrome and related intellectual disability (ID)/autism syndromes, emphasizing its key role in development. However, little is know on its complexity of interactions and functions in developmental processes. Here we show that loss of SIN-3, the single SIN3 homologue in Caenorhabditis elegans, results in maternal effect sterility associated with deregulation of the germline transcriptome, including derepression of X-linked genes. Using proteomics analysis we identify at least two SIN3 complexes containing distinct HDACs and differentially contributing to fertility. Single cell smFISH reveals that loss of sin-3 stochastically derepresses X linked genes in individual germ cells. We further identify acetylation marks whose abundance depends on SIN3. Together, this work provides a powerful paradigm for the in vivo study of SIN3 and associated proteins.
ORGANISM(S): Caenorhabditis elegans
PROVIDER: GSE227498 | GEO | 2023/10/04
REPOSITORIES: GEO
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