Opposing calcium-dependent signalling pathways control skeletal muscle differentiation by regulating a chromatin remodelling enzyme

Nasipak, Brian T.; Padilla‐Benavides, Teresita; Green, Karin M.; Leszyk, John D.; Mao, Wenjie; Konda, Silvana; Sif, Saı̈d; Shaffer, Scott A.; Ohkawa, Yasuyuki

doi:10.1038/ncomms8441

Cited by 41 publications

(89 citation statements)

References 60 publications

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“…Additionally, mammalian Brg1 is phosphorylated by PKC b1 and dephosphorylated by calcineurin to regulate skeletal muscle differentiation (Nasipak et al, 2015). Overall, our results support a conserved and integral role for SWI/SNF in mediating the transcriptional output of signaling cascades to facilitate cellular proliferation decisions.…”

Section: Discussionsupporting

confidence: 58%

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: 58%

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

Tsukiyama

2018

Preprint

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“…1). SMARCA4 is linked to calcium signaling (Lai et al 2009;Nasipak et al 2015). Literature also supports the idea that SMARCA4 (or the mammalian SWI/SNF complex) regulates lipid metabolism, as it was shown that SMARCA4 regulates PPARG expression, which in turn regulates lipid metabolism in differentiating adipocytes (Salma et al 2004).…”

Section: Discussionmentioning

confidence: 82%

SMARCA4 regulates gene expression and higher-order chromatin structure in proliferating mammary epithelial cells

et al. 2016

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The packaging of DNA into chromatin plays an important role in transcriptional regulation and nuclear processes. Brahmarelated gene-1 SMARCA4 (also known as BRG1), the essential ATPase subunit of the mammalian SWI/SNF chromatin remodeling complex, uses the energy from ATP hydrolysis to disrupt nucleosomes at target regions. Although the transcriptional role of SMARCA4 at gene promoters is well-studied, less is known about its role in higher-order genome organization. SMARCA4 knockdown in human mammary epithelial MCF-10A cells resulted in 176 up-regulated genes, including many related to lipid and calcium metabolism, and 1292 down-regulated genes, some of which encode extracellular matrix (ECM) components that can exert mechanical forces and affect nuclear structure. ChIP-seq analysis of SMARCA4 localization and SMARCA4-bound super-enhancers demonstrated extensive binding at intergenic regions. Furthermore, Hi-C analysis showed extensive SMARCA4-mediated alterations in higher-order genome organization at multiple resolutions. First, SMARCA4 knockdown resulted in clustering of intra-and inter-subtelomeric regions, demonstrating a novel role for SMARCA4 in telomere organization. SMARCA4 binding was enriched at topologically associating domain (TAD) boundaries, and SMARCA4 knockdown resulted in weakening of TAD boundary strength. Taken together, these findings provide a dynamic view of SMARCA4-dependent changes in higher-order chromatin organization and gene expression, identifying SMARCA4 as a novel component of chromatin organization.

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“…The myoblasts were contained in the lower interface of the 70% Percoll fraction and were washed with HBSS, centrifuged 5 min at 1,000 x g, and resuspended in growth media for plating. Myoblasts were grown and differentiated on plates coated with 0.02% collagen (Advanced BioMatrix) [119]. The different treatments (indicated in the figures) were: proliferation and differentiation (24 h).…”

Section: Primary Cell Culturementioning

confidence: 99%

MTF1, a classic metal sensing transcription factor, promotes myogenesis in response to copper

Tavera-Montañez

Cangussu

et al. 2019

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MTF1 is a conserved metal-binding transcription factor in eukaryotes that binds to conserved DNA sequence motifs, termed metal response elements (MREs). MTF1 responds to metal excess and deprivation, protects cells from oxidative and hypoxic stresses, and is required for embryonic development in vertebrates. We used multiple strategies to identify an unappreciated role for MTF1 and copper (Cu) in cell differentiation. Upon initiation of myogenesis from primary myoblasts, MTF1 expression increased, as did nuclear localization. Mtf1 knockdown impaired differentiation, while addition of non-toxic concentrations of Cu + enhanced MTF1 expression and promoted myogenesis. Cu + bound stoichiometrically to a Cterminus tetra-cysteine of MTF1. MTF1 bound to chromatin at the promoter regions of myogenic genes and binding was stimulated by copper. MTF1 formed a complex with MyoD at myogenic promoters, the master transcriptional regulator of the myogenic lineage. These studies establish novel mechanisms by which copper and MTF1 regulate gene expression in myoblast differentiation.

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Opposing calcium-dependent signalling pathways control skeletal muscle differentiation by regulating a chromatin remodelling enzyme

Cited by 41 publications

References 60 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

SMARCA4 regulates gene expression and higher-order chromatin structure in proliferating mammary epithelial cells

MTF1, a classic metal sensing transcription factor, promotes myogenesis in response to copper

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