The SWI/SNF chromatin-remodeling factors BAF60a, b, and c in nutrient signaling and metabolic control

Wang, Ruo-Ran; Pan, Ran; Zhang, Wenjing; Fu, Junfen; Lin, Jiandie D.; Meng, Zhuo

doi:10.1007/s13238-017-0442-2

Cited by 33 publications

(28 citation statements)

References 84 publications

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“…Our data demonstrate that SWI/SNF directly promotes the transition through the diauxic shift by activating transcription of required genes. This finding is consistent with known roles for SWI/SNF in regulating transcription of stress response genes and metabolic transitions in both yeast and mammals (Dutta et al, 2014;Erkina et al, 2008;Erkina et al, 2010;Neigeborn and Carlson, 1984;Shivaswamy and Iyer, 2008;Wang et al, 2018).…”

Section: Discussionsupporting

confidence: 88%

“…In support of these results, the Snf6 subunit of the SWI/SNF complex was shown to be required for Q cell formation (Li et al, 2015), and Snf2 was predicted to be a quiescence specific transcription factor by computational analyses (Reimand et al, 2012). Additionally, the SWI/SNF complex is a well-established regulator of transcription, known for activating glucose-repressed genes (Abrams et al, 1986) and genes involved in metabolic regulation and/or stress through its nucleosome remodeling activity (Awad et al, 2017;Côté et al, 1994;Dutta et al, 2014;Erkina et al, 2008;Geng and Laurent, 2004;Peterson et al, 1994;Qiu et al, 2016;Shivaswamy and Iyer, 2008;Wang et al, 2018).…”

Section: Snf2 Is Required For Q Entrymentioning

confidence: 99%

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SWI/SNF coordinates transcriptional activation through Rpd3-mediated histone hypoacetylation during quiescence entry

Tsukiyama

2018

Preprint

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Whether or not a cell chooses to divide is a tightly regulated and extremely important decision. Cells from yeast to human are able to reversibly exit the cell cycle in response to environmental changes such as nutritional changes or removal of growth cues to become quiescent. An inappropriate response to environmental cues can result in overproliferation which can lead to cancer, or a failure to proliferate which can result in developmental defects, premature aging and defects in wound healing. While many of the cell signaling pathways involved in regulating cellular quiescence have been identified, how these pathways translate their messages into transcriptional outputs is not well characterized. We previously showed that the histone deacetylase Rpd3 mediates global histone deacetylation and transcription repression upon quiescence entry. How the activation of quiescence-specific genes occurs in the midst of this transcriptionally repressive environment is not well understood. We show that the SWI/SNF chromatin remodeling complex activates quiescence specific genes to promote entry into quiescence. We additionally show that SWI/SNF binding early during quiescence entry is important for facilitating localization of the transcriptional activator Gis1, as well as histone H4 hypoacetylation in coding regions later on. The increase in H4 acetylation that we observe at Snf2-regulated genes upon Snf2 depletion corresponds to a decrease in promoter-bound Rpd3, suggesting that Snf2 remodels chromatin not only to facilitate activator binding, but also the binding of Rpd3. These observations provide mechanistic insight as to how quiescence-specific genes can be activated in the face of global deacetylation and transcription repression.

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Section: Discussionsupporting

confidence: 88%

Section: Snf2 Is Required For Q Entrymentioning

confidence: 99%

SWI/SNF coordinates transcriptional activation through Rpd3-mediated histone hypoacetylation during quiescence entry

Tsukiyama

2018

Preprint

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“…(8,9) In addition, chromatin-remodeling complexes and histone-and DNA-modifying enzymes act in concert with transcription factors to fine-tune gene expression. (10)(11)(12) Hepatic gene expression is exquisitely responsive to nutritional and hormonal signals and undergoes reprogramming in disease states such as NAFLD. Recent transcriptomic and proteomic studies have delineated a core molecular signature of diet-induced NASH in mice (13,14) and in human NASH livers.…”

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confidence: 99%

hnRNPU/TrkB Defines a Chromatin Accessibility Checkpoint for Liver Injury and Nonalcoholic Steatohepatitis Pathogenesis

et al. 2020

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Background and Aims Nonalcoholic steatohepatitis (NASH) is a progressive liver disease that is characterized by liver injury, inflammation, and fibrosis. NASH pathogenesis is linked to reprogramming of chromatin landscape in the liver that predisposes hepatocytes to stress‐induced tissue injury. However, the molecular nature of the putative checkpoint that maintains chromatin architecture and preserves hepatocyte health remains elusive. Approach and Results Here we show that heterogeneous nuclear ribonucleoprotein U (hnRNPU), a nuclear matrix protein that governs chromatin architecture and gene transcription, is a critical factor that couples chromatin disruption to NASH pathogenesis. RNA‐seq and chromatin immunoprecipitation‐seq studies revealed an extensive overlap between hnRNPU occupancy and altered gene expression during NASH. Hepatocyte‐specific inactivation of hnRNPU disrupted liver chromatin accessibility, activated molecular signature of NASH, and sensitized mice to diet‐induced NASH pathogenesis. Mechanistically, hnRNPU deficiency stimulated the expression of a truncated isoform of TrkB (TRKB‐T1) that promotes inflammatory signaling in hepatocytes and stress‐induced cell death. Brain‐derived neurotrophic factor treatment reduced membrane TRKB‐T1 protein and protected mice from diet‐induced NASH. Conclusions These findings illustrate a mechanism through which disruptions of chromatin architecture drive the emergence of disease‐specific signaling patterns that promote liver injury and exacerbate NASH pathogenesis.

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“…As SWI/SNF CRC is involved in sucrose metabolism in yeast, and in the regulation of nutrient sensing and metabolism control in mammals, we assessed the potential correlation of SMARCA2 expression with expression of genes coding for main glucose metabolism enzymes including: FBP1 (fructose‐1,6‐ bisphospatase) , GAPDH (glyceraldehyde 3‐phosphate dehydrogenase), ENO1 (enolase1) , LDHA (lactate dehydrogenase) , PKM2 (pyruvate kinase M) , ALDOA, ALDOB, ALDOC (aldolase A, B and C), and IDH1 (isocitrate dehydrogenase 1)—a Krebs cycle gene as well as PRKAA1 gene encoding the AMPKα1 subunit of AMP‐activated Protein Kinase (AMPK), the evolutionarily conserved ancient gauge of metabolism. The statistically significant correlation between expression of SMARCA2 and PKM 2 and PRKAA1 genes were found (Figure a).…”

Section: Resultsmentioning

confidence: 99%

“…SWI/SNF complex is known as sucrose metabolism regulator in yeast. In human cells, SWI/SNF CRCs control lipid metabolism, nutrient metabolism, and signaling . Therefore, we assessed the association of SMARCA2 expression with the main glucose metabolism genes.…”

Section: Discussionmentioning

confidence: 99%

SWI/SNF chromatin remodeling complex and glucose metabolism are deregulated in advanced bladder cancer

et al. 2020

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Bladder cancer (BC) is a frequently diagnosed malignancy affecting predominantly adult and elderly populations. It is expected that due to the longer life time, BC will become even more frequent in the future; thus in consequence, it will represent serious health problem of older society part. The treatment of advanced BC is mostly ineffective due to its very aggressive behavior. So far, no effective targeted therapy is used for BC treatment. Here, we found that BC is characterized by lower protein levels of BRM, INI1, and BAF155 main subunits of SWI/SNF chromatin remodeling complex (CRC) which is involved in global control of gene expression and influences various important cellular processes like: cell cycle control, apoptosis, DNA repair, etc. Moreover, the expression of SMARCA2, a BRM encoding gene, strongly correlated with BC metastasis and expression of such metabolic genes as PKM2 and PRKAA1. Furthermore, the analysis of T24 and 5637 commonly used BC cell lines revealed different expression levels of metabolic genes including FBP1 gene encoding Frutose-1,6-Bisphosphatase, an enzyme controlling glycolysis flux and gluconeogenesis. The tested BC cell lines exhibited various molecular and metabolic alterations as well as differential glucose uptake, growth rate, and migration potential. We have shown that BRM subunit is involved in the transcriptional control of genes encoding metabolic enzymes.Moreover, we found that the FBP1 expression level and the SWI/SNF CRCs may serve as markers of molecular subtypes of BC. Collectively, this study may provide a new knowledge about the molecular and metabolic BC subtypes which likely will be of high importance for the clinic in the future.

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The SWI/SNF chromatin-remodeling factors BAF60a, b, and c in nutrient signaling and metabolic control

Cited by 33 publications

References 84 publications

SWI/SNF coordinates transcriptional activation through Rpd3-mediated histone hypoacetylation during quiescence entry

SWI/SNF coordinates transcriptional activation through Rpd3-mediated histone hypoacetylation during quiescence entry

hnRNPU/TrkB Defines a Chromatin Accessibility Checkpoint for Liver Injury and Nonalcoholic Steatohepatitis Pathogenesis

SWI/SNF chromatin remodeling complex and glucose metabolism are deregulated in advanced bladder cancer

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