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SIN3 acts in distinct complexes to regulate the germline transcriptional program in C. elegans [sin-3(syb2172) and hda-3(ok1991)]

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: GSE227368 | GEO | 2023/10/04

REPOSITORIES: GEO

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SIN3 acts in distinct complexes to regulate the germline transcriptional program in C. elegans [sin-3(tm1276)]

Project description: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.

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MS-based proteomic characterization of SIN3-containing complexes in C. elegans

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SIN3 acts in distinct complexes to regulate the germline transcriptional program in C. elegans [sin-3(syb2172) and hda-3(ok1991)]

Project description:SIN3 acts in distinct complexes to regulate the germline transcriptional program in C. elegans [sin-3(syb2172) and hda-3(ok1991)]

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A role for mammalian Sin3 in permanent gene silencing

Project description:The multi-subunit Sin3 co-repressor complex regulates gene transcription through deacetylation of nucleosomes. However, the full range of Sin3 activities and targets is not well understood. Here, we have investigated genome-wide binding of mouse Sin3 and RBP2 as well as histone modifications and nucleosome positioning as a function of myogenic differentiation. Remarkably, we find that Sin3 complexes spread immediately downstream of the transcription start site on repressed and transcribed genes during differentiation. We show that RBP2 is part of a Sin3 complex, and on a subset of E2F4 target genes, the coordinated activity of Sin3 and RBP2 leads to deacetylation, demethylation, and repositioning of nucleosomes. Our work provides evidence for coordinated binding of Sin3, chromatin modifications, and chromatin remodeling within discrete regulatory regions, suggesting a model in which spreading of Sin3 binding is ultimately linked to permanent gene silencing on a subset of E2F4 target genes.

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SIN3 acts in distinct complexes to regulate the germline transcriptional program in C. elegans [sin-3(tm1276)]

Project description:SIN3 acts in distinct complexes to regulate the germline transcriptional program in C. elegans [sin-3(tm1276)]

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Mapping binding sites of SIN3 isoforms across the Drosophila genome.

Project description:SIN3 associates with RPD3 and other accessory proteins to form the SIN3 histone modifying complex. A single Sin3A gene encodes multiple SIN3 isoforms, of which SIN3 187 and SIN3 220 are predominant. Previous studies from our laboratory and others have indicated that SIN3 isoforms play non-redundant roles during fly development, however, the genes regulated by SIN3 isoforms are not known. We mapped the genome-wide binding sites of SIN3 isoforms in Drosophila. We established stable S2 cell lines that express either HA-tagged SIN3 187 or SIN3 220. The binding profiles revealed that the majority of the binding sites of SIN3 isoforms are overlapping. Our data revealed that SIN3 isoforms localize to euchromatic regions of the genome and enrichment of SIN3 isoforms are generally concentrated around the transcription start sites of genes. In addition, the extent of SIN3 binding confirmed previous findings indicating that SIN3 is a global transcriptional regulator.

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Mapping binding sites of SIN3 isoforms across the Drosophila genome.

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Transcriptome analysis upon overexpression of SIN3 187HA in Drosophila cultured cells

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Transcriptome analysis upon overexpression of SIN3 187HA in Drosophila cultured cells

Project description:SIN3 is a master transcriptional scaffold protein. SIN3 interacts with RPD3 and other accessory proteins to form a histone modifying complex. A single Sin3A gene encodes multiple isoforms of SIN3, of which SIN3 187 and SIN3 220 are the predominant isoforms. Previous studies demonstrated that SIN3 isoforms play non-redundant roles during fly development. In the current study, we sought to investigate the genes regulated by SIN3 187. S2 cells and cells carrying a stable transgene of SIN3 187HA (SIN3 187HA cells) were treated with 0.07 ÂµM CuSO4. CuSO4 treatment led to ectopic expression of SIN3 187HA. S2 cells were used as a control. Following induction, total mRNA was extracted. mRNA profiling of these samples were performed by deep sequencing using Illumina Hiseq2500. Three biological replicates were performed.

2016-01-09 | E-GEOD-72172 | biostudies-arrayexpress

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