The histone modification regulator, SIN3, plays a role in the cellular response to changes in glycolytic flux

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The paper studied how the epigenetic regulator SIN3 influences gene expression programs involved in central carbon metabolism when cells experience changes in metabolic flux. Using experimental approaches including loss of SIN3, the authors report that SIN3 regulatory action affects a subset of metabolic genes and that SIN3 loss is associated with decreased mitochondrial respiration and altered responses to both mitochondrial and glycolytic stress. The paper’s major caveat is that the abstract provides evidence linking SIN3 to metabolic-flux responsive gene regulation, but it does not specify the breadth of mechanisms beyond these measured outcomes in the text provided. This paper does not explicitly discuss endometriosis or adenomyosis; it was included in the corpus via a keyword match in the upstream search index.

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Abstract

Epigenetic regulation and metabolism are connected. Epigenetic regulators, like the SIN3 complex, affect the expression of a wide range of genes, including those encoding metabolic enzymes essential for central carbon metabolism. The idea that epigenetic modifiers can sense and respond to metabolic flux by regulating gene expression has long been proposed. In support of this cross-talk, we provide data linking SIN3 regulatory action on a subset of metabolic genes with the cellular response to changes in metabolic flux. Furthermore, we show that loss of SIN3 is linked to decreases in mitochondrial respiration and the cellular response to mitochondrial and glycolytic stress. Data presented here provide evidence that SIN3 is important for the cellular response to metabolic flux change.
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Abstract Epigenetic regulation and metabolism are connected. Epigenetic regulators, like the SIN3 complex, affect the expression of a wide range of genes, including those encoding metabolic enzymes essential for central carbon metabolism. The idea that epigenetic modifiers can sense and respond to metabolic flux by regulating gene expression has long been proposed. In support of this cross-talk, we provide data linking SIN3 regulatory action on a subset of metabolic genes with the cellular response to changes in metabolic flux. Furthermore, we show that loss of SIN3 is linked to decreases in mitochondrial respiration and the cellular response to mitochondrial and glycolytic stress. Data presented here provide evidence that SIN3 is important for the cellular response to metabolic flux change. Competing Interest Statement The authors have declared no competing interest. - SAM - S-adenosylmethionine - H3K9ac - Histone H3 lysine 9 acetylation - TSS - Transcription Start Site - KAT - lysine histone acetylase - HDAC - Histone Deacetylase - TCA cycle - Tricarboxylic Acid Cycle - 2-DG - 2-Deoxy-D-glucose - RNAi - RNA interference - qPCR - quantitative PCR

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europepmc
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License: CC-BY-4.0