ArticleDevelopment (Cambridge, England)2023
SIN-3 acts in distinct complexes to regulate the germline transcriptional program in Caenorhabditis elegans.
Article in Development (Cambridge, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 3 citations in OpenAlex.
- HDAC1/2-mediated repression of Wnt receptor expression orients asymmetric division polarity in Caenorhabditis elegans.Development (Cambridge, England) · 2026Article
- Developmental priming of adult proteostasis and longevity by NuA4 complex activity in early life.The EMBO journal · 2026Article
- SIN-3 coregulator maintains adaptive capacity to different diets in Caenorhabditis elegans through vitamin B12.G3 (Bethesda, Md.) · 2026Article
- Histone deacetylase inhibition expands cellular proteostasis repertoires to enhance neuronal stress resilience.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
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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 fertility. Single-cell, single-molecule fluorescence in situ hybridization reveals that in sin-3 mutants the X chromosome becomes re-expressed prematurely and in a stochastic manner in individual germ cells, suggesting a role for SIN-3 in its silencing. Furthermore, we identify histone residues whose acetylation increases in the absence of SIN-3. Together, this work provides a powerful framework for the in vivo study of SIN3 and associated proteins.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.