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The Swi-Snf chromatin remodeling complex mediates gene activation through metabolic control [RNA-seq I]

ABSTRACT: In eukaryotes, ATP-dependent chromatin remodelers regulate gene expression in response to nutritional and metabolic stimuli. The Swi-Snf complex is one such remodeler that has been implicated in disease, where loss of Swi-Snf function leads to dysregulated gene transcription. However, altered transcription of metabolic genes may have consequences for entire pathways that remain poorly understood. In this study, we use genetic and molecular approaches to uncover a role for Swi-Snf as a critical regulator of metabolism. We find that Δsnf mutants are cysteine-deficient, despite growth in nutrient-rich media. This cysteine deficiency causes widespread perturbations in sulfur metabolic gene transcription. This includes global alteration and redistribution of the transcription factor Met4 which senses cysteine deficiency and also has roles in heavy metal stress response and cell cycle progression. Additionally, we show that in its role as a metabolic regulator, Swi-Snf is a critical determinant of survival following oxidative stress. Our findings show how a chromatin remodeler can have a significant impact on a whole metabolic pathway by directly regulating an important gene subset and demonstrate an emerging role for chromatin remodeling complexes as key determinants of metabolic control.

ORGANISM(S): Saccharomyces cerevisiae

PROVIDER: GSE197918 | GEO | 2023/08/22

REPOSITORIES: GEO

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The Swi-Snf chromatin remodeling complex mediates gene activation through metabolic control [RNA-Seq II]

Project description:In eukaryotes, ATP-dependent chromatin remodelers regulate gene expression in response to nutritional and metabolic stimuli. The Swi-Snf complex is one such remodeler that has been implicated in disease, where loss of Swi-Snf function leads to dysregulated gene transcription. However, altered transcription of metabolic genes may have consequences for entire pathways that remain poorly understood. In this study, we use genetic and molecular approaches to uncover a role for Swi-Snf as a critical regulator of metabolism. We find that Δsnf mutants are cysteine-deficient, despite growth in nutrient-rich media. This cysteine deficiency causes widespread perturbations in sulfur metabolic gene transcription. This includes global alteration and redistribution of the transcription factor Met4 which senses cysteine deficiency and also has roles in heavy metal stress response and cell cycle progression. Additionally, we show that in its role as a metabolic regulator, Swi-Snf is a critical determinant of survival following oxidative stress. Our findings show how a chromatin remodeler can have a significant impact on a whole metabolic pathway by directly regulating an important gene subset and demonstrate an emerging role for chromatin remodeling complexes as key determinants of metabolic control.

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The Swi-Snf chromatin remodeling complex mediates gene activation through metabolic control [ChIP-seq]

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SWI/SNF is positively auto-regulated by an AT-hook in the catalytic subunit

Project description:The SWI/SNF ATP-dependent chromatin remodeler is a master regulator of the epigenome; controlling pluripotency, cell fate determination and differentiation. There is a sparsity of information on the autoregulation of SWI/SNF, the domains involved and their mode of action. We find a DNA or RNA binding module conserved from yeast to humans located in the C-terminus of the catalytic subunit of SWI/SNF called the AT-hook that positively regulates the chromatin remodeling activity of yeast and mouse SWI/SNF. The AT-hook in yeast SWI/SNF interacts with the SnAC and ATPase domains, which after binding to nucleosome switches to contacting the N-terminus of histone H3. Deletion of the AT-hooks in yeast SWI/SNF and mouse esBAF complexes reduces the remodeling activity of SWI/SNF without affecting complex integrity or its recruitment to nucleosomes. In addition, deletion of the AT-hook impairs the ATPase and nucleosome mobilizing activities of yeast SWI/SNF without disrupting the interactions of the ATPase domain with nucleosomal DNA. The AT-hook is also important in vivo for SWI/SNF-dependent response to amino acid starvation in yeast and for cell lineage priming in mouse embryonic stem cells. In summary, the AT-hook is shown to be an evolutionarily conserved autoregulatory domain of SWI/SNF that positively regulates SWI/SNF both in vitro and in vivo.

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Genome-wide profile of the SWI/SNF chromatin remodeling complex

Project description:A systems understanding of nuclear organization and events is critical for determining how cells divide, differentiate and respond to stimuli and for identifying the causes of diseases. Chromatin remodeling complexes such as SWI/SNF have been implicated in a wide variety of cellular processes including gene expression, nuclear organization, centromere function and chromosomal stability, and mutations in SWI/SNF components have been linked to several types of cancer. To better understand the biological processes in which chromatin remodeling proteins participate we globally mapped binding regions for several components of the SWI/SNF complex throughout the human genome using ChIP-Seq. SWI/SNF components were found to lie near regulatory elements integral to transcription (e.g. 5M-bM-^@M-^Y ends, RNA Polymerases II and III and enhancers) as well as regions critical for chromosome organization (e.g. CTCF, lamins and DNA replication origins). To further elucidate the association of SWI/SNF subunits with each other as well as with other nuclear proteins we also analyzed SWI/SNF immunoprecipitated complexes by mass spectrometry. Individual SWI/SNF factors are associated with their own family members as well as with cellular constituents such as nuclear matrix proteins, key transcription factors and centromere components implying a ubiquitous role in gene regulation and nuclear function. We find an overrepresentation of both SWI/SNF-associated regions and proteins in cell cycle and chromosome organization. Taken together the results from our ChIP and immunoprecipitation experiments suggest that SWI/SNF facilitates gene regulation and genome function more broadly and through a greater diversity of interactions than previously appreciated. ChIP-Seq analysis of the SWI/SNF subunits Ini1, Brg1, BAF155 and BAF170 in HeLa S3 cells

2011-01-10 | E-GEOD-24397 | biostudies-arrayexpress

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