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The chromatin factors SET-26 and HCF-1 oppose the histone deacetylase HDA-1 in longevity and gene regulation in C. elegans [RNA-Seq]

ABSTRACT: SET-26, HCF-1, and HDA-1 are highly conserved chromatin factors with key roles in development and aging. Here we present mechanistic insights into how these factors regulate gene expression and modulate longevity in C. elegans. We show that SET-26 and HCF-1 cooperate to regulate a common set of genes, and both antagonize the histone deacetylase HDA-1 to limit longevity. We propose a model in which SET-26 recruits HCF-1 to chromatin in somatic cells, where they stabilize each other at the promoters of a subset of genes, particularly mitochondrial function genes, and regulate their expression. HDA-1 opposes SET-26 and HCF-1 on the regulation of a subset of their common target genes and in longevity. Our findings suggest that SET-26, HCF-1, and HDA-1 comprise a mechanism to fine-tune gene expression and longevity and likely have important implications for the mechanistic understanding of how these factors function in diverse organisms, particularly in aging biology.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE224075 | GEO | 2024/01/29

REPOSITORIES: GEO

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The chromatin factors SET-26 and HCF-1 oppose the histone deacetylase HDA-1 in longevity and gene regulation in C. elegans [CUT&RUN]

Project description:SET-26, HCF-1, and HDA-1 are highly conserved chromatin factors with key roles in development and aging. Here we present mechanistic insights into how these factors regulate gene expression and modulate longevity in C. elegans. We show that SET-26 and HCF-1 cooperate to regulate a common set of genes, and both antagonize the histone deacetylase HDA-1 to limit longevity. We propose a model in which SET-26 recruits HCF-1 to chromatin in somatic cells, where they stabilize each other at the promoters of a subset of genes, particularly mitochondrial function genes, and regulate their expression. HDA-1 opposes SET-26 and HCF-1 on the regulation of a subset of their common target genes and in longevity. Our findings suggest that SET-26, HCF-1, and HDA-1 comprise a mechanism to fine-tune gene expression and longevity and likely have important implications for the mechanistic understanding of how these factors function in diverse organisms, particularly in aging biology.

2024-01-29 | GSE224076 | GEO

The chromatin factors SET-26 and HCF-1 oppose the histone deacetylase HDA-1 in longevity and gene regulation in C. elegans

Project description:In this study, a GFP-tagged version of the protein HCF-1 was immuno-precipitated from C. elegans lysates of the strain IU171 and co-purifying proteins were identified by LC-MS/MS. As a negative control, the same immuno-precipitation was conducted from wild-type (strain N2) worms that did not carry a HCF-1::GFP transgene.

2024-01-29 | PXD047509 | Pride

DVE-1_ChIP-seq and HDA-1_ChIP-seq of worms

Project description:Mitochondria are important organelles, but their function is often challenged by toxic products of metabolism as well as by pathogen attack. The mitochondrial unfolded protein response (UPRmt) monitors mitochondrial function in general: it is responsible for buffering the mitochondrial protein folding environment, and controlling mitochondria-nuclear balance of the electron transport chain (ETC) components. Besides, UPRmt plays essential roles in aging and lifespan. Here we found that knocking down histone deacetylase hda-1 robustly attenuated UPRmt and lifespan extension. We identified HDA-1 as a required factor for UPRmt activation and HDA-1 is associated with the homeobox domain-containing protein DVE-1.So, we performed ChIP-seq of worms to find DNA regions on which HDA-1 and DVE-1 bound, and if their binding depend on each other.

2020-07-19 | GSE141042 | GEO

hcf-1(-) transcriptional profiling

Project description:We used microarrays to identify genes regulated by HCF-1 in a daf-16-dependent manner. Samples from young adult worms were hybridized to Agilent microarrays to identify genes differentially expressed in hcf-1(pk924)/daf-16(mgDf47);hcf-1(pk924) and compared to hcf-1(pk924)/N2 arrays.

2011-07-22 | E-GEOD-30725 | biostudies-arrayexpress

SET-9 and SET-26 are H3K4me3 readers and play critical roles in germline development and longevity

Project description:SET-9 and SET-26 are highly homologous paralogs that share redundant function in germline development, but SET-26 alone plays a key role in longevity and heat stress response. SET-26 is broadly expressed, but SET-9 is only detectable in the germline, which likely account for their different biological roles. SET-9 and SET-26 bind to H3K4me3 in vitro and in vivo, and their loss results in broadening of H3K4me3 domains. SET-9 and SET-26 also regulate the RNA expression of a subset of their target genes, irrespective of their H3K4me3 status. We propose that SET-9 and SET-26 function to organize local chromatin environment and to regulate the expression of specific target genes, and these activities together contribute to their critical roles in germline development, stress response, and longevity. SET-9 and SET-26 are highly homologous to human MLL5, a factor implicated in leukemia and glioblastoma, and our findings help to provide new insights into MLL5.

2018-05-31 | GSE108848 | GEO

SET-9 and SET-26, the C. elegans homologs of human MLL5, are critical for germline development and longevity

2018-05-31 | GSE100623 | GEO

hcf-1(-) transcriptional profiling

Project description:We used microarrays to identify genes regulated by HCF-1 in a daf-16-dependent manner.

2011-07-23 | GSE30725 | GEO

Rapid recapitulation of non-alcoholic steatohepatitis upon loss of HCF-1 function in mouse hepatocytes [ChIP-seq]

Project description:Background and Aims: Host-cell factor 1 (HCF-1), encoded by the ubiquitously expressed X linked gene Hcfc1, is an epigenetic co-regulator important for mouse development and cell proliferation, including during liver regeneration. Here, we examine the role of HCF-1 in adult tissue physiology using, as model, the resting mouse liver. Methods: We used a hepatocyte-specific inducible Hcfc1 knock-out allele (called Hcfc1hepKO), to induce HCF-1 loss in hepatocytes of hemizygous Hcfc1 hepKO/Y males by four days. In heterozygous Hcfc1hepKO/+ females, owing to random X-chromosome inactivation, upon Hcfc1hepKO allele induction, a 50/50 mix of HCF-1 positive and negative hepatocyte clusters is engineered. Results: The livers with Hcfc1hepKO/Y hepatocytes displayed a 21 24-day terminal non-alcoholic fatty liver (NAFL) followed by non-alcoholic steatohepatitis (NASH) disease progression typical of severe NAFL disease (NAFLD). In contrast, in livers with heterozygous Hcfc1hepKO/+ hepatocytes, HCF-1-positive hepatocytes replaced HCF-1-negative hepatocytes and revealed only mild-NAFL development. Loss of HCF-1 led to loss of PGC1 alpha protein levels, probably owing to its destabilization, and deregulation of gene expression particularly of genes involved in mitochondrial structure and function, likely explaining the severe Hcfc1hepKO/Y liver pathology. Interestingly, although HCF-1 binds to over 5000 transcriptional start sites in the resting liver, expression of only a minor subset of the associated genes was affected by HCF-1 loss. Conclusion: HCF-1 is essential for proper liver physiology likely playing both transcriptional and non-transcriptional roles. These genetically-engineered loss-of-HCF-1 mice represent models for the study of NASH and NAFLD resolution.

2019-02-27 | GSE115767 | GEO

Rapid recapitulation of non-alcoholic steatohepatitis upon loss of HCF-1 function in mouse hepatocytes [RNA-seq]

Project description:Background and Aims: Host-cell factor 1 (HCF-1), encoded by the ubiquitously expressed X linked gene Hcfc1, is an epigenetic co-regulator important for mouse development and cell proliferation, including during liver regeneration. Here, we examine the role of HCF-1 in adult tissue physiology using, as model, the resting mouse liver. Methods: We used a hepatocyte-specific inducible Hcfc1 knock-out allele (called Hcfc1hepKO), to induce HCF-1 loss in hepatocytes of hemizygous Hcfc1 hepKO/Y males by four days. In heterozygous Hcfc1hepKO/+ females, owing to random X-chromosome inactivation, upon Hcfc1hepKO allele induction, a 50/50 mix of HCF-1 positive and negative hepatocyte clusters is engineered. Results: The livers with Hcfc1hepKO/Y hepatocytes displayed a 21–24-day terminal non-alcoholic fatty liver (NAFL) followed by non-alcoholic steatohepatitis (NASH) disease progression typical of severe NAFL disease (NAFLD). In contrast, in livers with heterozygous Hcfc1hepKO/+ hepatocytes, HCF-1-positive hepatocytes replaced HCF-1-negative hepatocytes and revealed only mild-NAFL development. Loss of HCF-1 led to loss of PGC1 alpha protein levels, probably owing to its destabilization, and deregulation of gene expression particularly of genes involved in mitochondrial structure and function, likely explaining the severe Hcfc1hepKO/Y liver pathology. Interestingly, although HCF-1 binds to over 5000 transcriptional start sites in the resting liver, expression of only a minor subset of the associated genes was affected by HCF-1 loss. Conclusion: HCF-1 is essential for proper liver physiology likely playing both transcriptional and non-transcriptional roles. These genetically-engineered loss-of-HCF-1 mice represent models for the study of NASH and NAFLD resolution.

2019-02-27 | GSE115766 | GEO

The effect of doxycycline-induced expression of host-cell-factor 2 (HCF-2) proteins on the global gene expression in HEK-293 cells

Project description:Here we study the effect of doxycycline induced expression of HCF-2 (the host-cell-factor 2) proteins - HCF-2WT and its mutant HCF-2Fn3nc* on the global gene expression in HEK-293 cells. We identified 7175 genes that were differentially expressed after day 1 in any of the HCF-2WT or HCF-2Fn3nc* samples (log2 (fold change) > 0.5 or < -0.5 and FDR < 0.05). The maximal gene-expression changes over time were on day 6 in each case, with more genes up-regulated (2199 vs. 1241) in the HCF-2WT samples and more genes down-regulated (2513 vs. 1555) in the HCF-2Fn3nc* samples after six days compared to day 1. Notably, there was little overlap between the genes affected by the induced synthesis of HCF-2WT or HCF-2Fn3nc* indicating that the HCF-2Fn3nc* mutation seriously disrupts HCF-2 function. In total, we found that up-regulated genes in HCF-2WT were associated with developmental and morphogenesis programs induction, whereas down-regulated genes were linked to the inhibition of cellular metabolism and proliferation.

2019-04-17 | GSE128076 | GEO

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