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Short Chain Fatty Acid Independent Hepatic Histone Acetylation Patterns, Induced by Microbiota Exposure, are Irreversible

ABSTRACT: Short Chain Fatty Acid Independent Hepatic Histone Acetylation Patterns, Induced by Microbiota Exposure, are Irreversible

PROVIDER: PRJNA603270 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10969116.fastq.gz	Fastqsanger.gz
	SRR10969117.fastq.gz	Fastqsanger.gz
	SRR10969118.fastq.gz	Fastqsanger.gz
	SRR10969119.fastq.gz	Fastqsanger.gz
	SRR10969120.fastq.gz	Fastqsanger.gz

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Short Chain Fatty Acid Independent Hepatic Histone Acetylation Patterns, Induced by Microbiota Exposure, are Irreversible

Project description:Germ-free mice are an indispensable tool in studying the gut microbiome and its effects on host physiology, though they are phenotypically different than their conventional counterparts. While antibiotic mediated microbiota depletion in conventional mice mimics the germ-free state, the scope of these reversible changes is unknown. We demonstrate robust hepatic transcriptomic alterations after antibiotic-mediated microbiota depletion together with depletion of luminal and portal vein levels of SCFAs though hepatic histone acetylation states remained largely unchanged.

2023-01-25 | GSE144266 | GEO

Global Microbiota-Dependent Histone Acetylation Patterns Are Irreversible and Independent of Short Chain Fatty Acids.

Project description:Background and aimsAlthough germ-free mice are an indispensable tool in studying the gut microbiome and its effects on host physiology, they are phenotypically different than their conventional counterparts. While antibiotic-mediated microbiota depletion in conventional mice leads to physiologic alterations that often mimic the germ-free state, the degree to which the effects of microbial colonization on the host are reversible is unclear. The gut microbiota produce abundant short chain fatty acids (SCFAs), and previous studies have demonstrated a link between microbial-derived SCFAs and global hepatic histone acetylation in germ-free mice.Approach and resultsWe demonstrate that global hepatic histone acetylation states measured by mass spectrometry remained largely unchanged despite loss of luminal and portal vein SCFAs after antibiotic-mediated microbiota depletion. In contrast to stable hepatic histone acetylation states, we see robust hepatic transcriptomic alterations after microbiota depletion. Additionally, neither dietary supplementation with supraphysiologic levels of SCFA nor the induction of hepatocyte proliferation in the absence of microbiota-derived SCFAs led to alterations in global hepatic histone acetylation.ConclusionsThese results suggest that microbiota-dependent landscaping of the hepatic epigenome through global histone acetylation is static in nature, while the hepatic transcriptome is responsive to alterations in the gut microbiota.

| S-EPMC9867598 | biostudies-literature

T Cell Genes Regulated by Short Chain Fatty Acids

Project description:This is to determine the regulation of gene expression in different T Cell population with short chain fatty acids. This will provide the roles of SCFAs in regulation of adaptive immunity and T-cell-mediated inflammation.

2018-06-13 | GSE31585 | GEO

Short-chain fatty acids improve post-stroke recovery via immunological mechanisms.

Project description:This transcriptomic study investigates the effect of therapeutic short-chain fatty acids (SCFA) administration on post-stroke recovery.

2020-01-01 | GSE131788 | GEO

Data for: Short-chain fatty acids activate acetyltransferase p300/CBP

Project description:The short-chain fatty acids (SCFAs) acetate, propionate, and butyrate are produced in large quantities by the gut microbiome and contribute to a wide array of physiological processes. While the underlying mechanisms are largely unknown, many effects of SCFAs have been traced to changes in epigenetic state. Here, we systematically investigate how SCFAs alter the epigenome. Using quantitative proteomics of histone modification states, we identified rapid and sustained increases in histone acetylation after addition of butyrate or propionate, but not acetate. While decades of prior observations would have suggested that hyperacetylation induced by SCFAs are attributed to inhibition of histone deacetylases (HDACs), we found that propionate and butyrate instead activate the acetyltransferase p300/CBP. Propionate and butyrate are rapidly converted to the corresponding acyl-CoAs which are then used by p300/CBP to catalyze auto-acylation of the autoinhibitory loop, activating the enzyme for histone/protein acetylation. This data challenges the long-held belief that SCFAs mainly regulate chromatin by inhibiting HDACs, and instead reveals a previously unappreciated mechanism of HAT activation that can explain how even low levels of SCFAs can alter epigenomes.

2021-07-12 | MSV000087800 | MassIVE

GNPS Data for: Short-chain fatty acids activate acetyltransferase p300/CBP

2021-07-12 | MSV000087800 | GNPS

Enterohemorrhagic Escherichia coli: impact of short chain fatty acid treatment on virulence gene expression

Project description:transcriptome analysis of enterohemorrhagic E. coli treated with either one of two different concentrations of short chain fatty acid mixes or the corresponding sodium chloride osmolarity control four conditions: 30mM SCFA mix; 30mM NaCl control; 172mM SCFA mix: 172 mM NaCl control. Biological replicates: 4 per group

2016-03-23 | E-GEOD-79509 | biostudies-arrayexpress

Short chain fatty acids induce ANGPTL4 via PPARγ

Project description:Angiopoietin-like protein 4 (ANGPTL4, also referred to as Fiaf) has been proposed as circulating mediator between the gut microbiota and fat storage in adipose tissue. Very little is known about mechanisms of regulation of ANGPTL4 in the colon. Here we show that transcription and subsequent secretion of ANGPTL4 in human T84 and HT-29 colonocytes is highly induced by physiological concentrations of products of bacterial fermentation, the short chain fatty acids (SCFA). Induction of ANGPTL4 by SCFA cannot be mimicked by the histone deacetylase inhibitor Trichostatin A. SCFA induce ANGPTL4 by activating the nuclear receptor PPARγ, as shown by use of PPARγ antagonist, PPARγ knock-down, and transactivation assay, which shows activation of PPARγ but not PPARα and PPARδ. At concentrations required for PPARγ activation and ANGPTL4 induction in colonocytes, SCFA do not stimulate PPARγ in mouse 3T3-L1 and human SGBS adipocytes, suggesting that SCFA act as selective PPARγ modulators (SPPARM), which is supported by coactivator peptide recruitment assay and structural modelling. Consistent with the notion that fermentation leads to PPAR activation in vivo, feeding mice a diet rich in inulin was associated with induction of PPAR target genes and pathways in the colon, as shown by microarray and subsequent gene set enrichment analysis. It can be concluded that 1) SCFA potently stimulate ANGPTL4 synthesis in human colonocytes; 2) SCFA transactivate and bind to PPARγ by serving as selective PPAR modulators. Our data point to activation of PPARγ as a novel mechanism of gene regulation by SCFA in the colon.

2013-03-11 | GSE43065 | GEO

ACSS2-mediated acetylation promotes BCAT1 aggradation to elevate branched-chain amino acid metabolism and development of pancreatic cancer

Project description:ACSS2-mediated acetylation promotes BCAT1 aggradation to elevate branched-chain amino acid metabolism and development of pancreatic cancer

2025-05-01 | GSE279400 | GEO