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SIN3 acts in distinct complexes to regulate the germline transcriptional program in C. elegans

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE227499 | 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.

2023-10-04 | GSE227498 | GEO

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

2023-10-04 | GSE227368 | GEO

SIN3 acts in distinct complexes to regulate the germline transcriptional program in C. elegans

Project description:SIN3 acts in distinct complexes to regulate the germline transcriptional program in C. elegans

| PRJNA945391 | ENA

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)]

| PRJNA945400 | ENA

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)]

| PRJNA944713 | ENA

GEMC1 and MCIDAS interactions with SWI/SNF complexes regulate the multiciliated cell-specific transcriptional program.

Project description:Multiciliated cells (MCCs) project dozens to hundreds of motile cilia from their apical surface to promote the movement of fluids or gametes in the mammalian brain, airway or reproductive organs. Differentiation of MCCs requires the sequential action of the Geminin family transcriptional activators, GEMC1 and MCIDAS, that both interact with E2F4/5-DP1. How these factors activate transcription and the extent to which they play redundant functions remains poorly understood. Here, we demonstrate that the transcriptional targets and proximal proteomes of GEMC1 and MCIDAS are highly similar. However, we identified distinct interactions with SWI/SNF subcomplexes; GEMC1 interacts primarily with the ARID1A containing BAF complex while MCIDAS interacts primarily with BRD9 containing ncBAF complexes. Treatment with a BRD9 inhibitor impaired MCIDAS-mediated activation of several target genes and compromised the MCC differentiation program in multiple cell based models. Our data suggest that the differential engagement of distinct SWI/SNF subcomplexes by GEMC1 and MCIDAS is required for MCC-specific transcriptional regulation and mediated by their distinct C-terminal domains.

| S-EPMC10023806 | biostudies-literature

C. elegans germ granules regulate both germline and somatic RNAome

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-07-20 | GSE228859 | GEO

LncRNA SCIRT acts in a negative feedback loop to regulate the transcriptional program for cancer self-renewal

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-02-23 | GSE136195 | GEO

The zinc-finger transcription factor LSL-1 is a major regulator of the germline transcriptional program in Caenorhabditis elegans.

Project description:Specific gene transcriptional programs are required to ensure the proper proliferation and differentiation processes underlying the production of specialized cells during development. Gene activity is mainly regulated by the concerted action of transcription factors and chromatin proteins. In the nematode Caenorhabditis elegans, mechanisms that silence improper transcriptional programs in germline and somatic cells have been well studied, however, how are tissue-specific sets of genes turned on is less known. LSL-1 is herein defined as a novel crucial transcriptional regulator of germline genes in C. elegans. LSL-1 is first detected in the P4 blastomere and remains present at all stages of germline development, from primordial germ cell proliferation to the end of meiotic prophase. lsl-1 loss-of-function mutants exhibit many defects including meiotic prophase progression delay, a high level of germline apoptosis, and production of almost no functional gametes. Transcriptomic analysis and ChIP-seq data show that LSL-1 binds to promoters and acts as a transcriptional activator of germline genes involved in various processes, including homologous chromosome pairing, recombination, and genome stability. Furthermore, we show that LSL-1 functions by antagonizing the action of the heterochromatin proteins HPL-2/HP1 and LET-418/Mi2 known to be involved in the repression of germline genes in somatic cells. Based on our results, we propose LSL-1 to be a major regulator of the germline transcriptional program during development.

| S-EPMC9071529 | biostudies-literature

Isoforms of the transcriptional cofactor SIN3 differentially regulate genes necessary for energy metabolism and cell survival.

Project description:The SIN3 scaffolding protein is a conserved transcriptional regulator known to fine-tune gene expression. In Drosophila, there are two major isoforms of SIN3, SIN3 220 and SIN3 187, which each assemble into multi-subunit histone modifying complexes. The isoforms have distinct developmental expression patterns and non-redundant functions. Gene regulatory network analyses indicate that both isoforms affect genes encoding proteins in pathways such as the cell cycle and cell morphogenesis. Interestingly, the SIN3 187 isoform uniquely regulates a subset of pathways including post-embryonic development, phosphate metabolism and apoptosis. Target genes in the phosphate metabolism pathway include nuclear-encoded mitochondrial genes coding for proteins responsible for oxidative phosphorylation. Here, we investigate the physiological effects of SIN3 isoforms on energy metabolism and cell survival. We find that ectopic expression of SIN3 187 represses expression of several nuclear-encoded mitochondrial genes affecting production of ATP and generation of reactive oxygen species (ROS). Forced expression of SIN3 187 also activates several pro-apoptotic and represses a few anti-apoptotic genes. In the SIN3 187 expressing cells, these gene expression patterns are accompanied with an increased sensitivity to paraquat-mediated oxidative stress. These findings indicate that SIN3 187 influences the regulation of mitochondrial function, apoptosis and oxidative stress response in ways that are dissimilar from SIN3 220. The data suggest that the distinct SIN3 histone modifying complexes are deployed in different cellular contexts to maintain cellular homeostasis.

| S-EPMC10557476 | biostudies-literature

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