scholarly journals NCAPG Dynamically Coordinates the Myogenesis of Fetal Bovine Tissue by Adjusting Chromatin Accessibility

2020 ◽  
Vol 21 (4) ◽  
pp. 1248
Author(s):  
Xin Hu ◽  
Yishen Xing ◽  
Xing Fu ◽  
Qiyuan Yang ◽  
Ling Ren ◽  
...  
Keyword(s):  
Gene Expression ◽  
High Throughput Sequencing ◽  
Myogenic Differentiation ◽  
Chromatin Condensation ◽  
Chromatin Accessibility ◽  
Myoblast Differentiation ◽  
Specific Gene ◽  
Specific Gene Expression ◽  
Bovine Tissue ◽  
Fetal Bovine

NCAPG is a subunit of condensin I that plays a crucial role in chromatin condensation during mitosis. NCAPG has been demonstrated to be associated with farm animal growth traits. However, its role in regulating myoblast differentiation is still unclear. We used myoblasts derived from fetal bovine tissue as an in vitro model and found that NCAPG was expressed during myogenic differentiation in the cytoplasm and nucleus. Silencing NCAPG prolonged the mitosis and impaired the differentiation due to increased myoblast apoptosis. After 1.5 days of differentiation, silencing NCAPG enhanced muscle-specific gene expression. An assay for transposase-accessible chromatin- high throughput sequencing (ATAC-seq) revealed that silencing NCAPG altered chromatin accessibility to activating protein 1 (AP-1) and its subunits. Knocking down the expression of the AP-1 subunits fos-related antigen 2 (FOSL2) or junB proto-oncogene (JUNB) enhanced part of the muscle-specific gene expression. In conclusion, our data provide valuable evidence about NCAPG’s function in myogenesis, as well as its potential role in gene expression.

scholarly journals Lens differentiation is characterized by stage-specific changes in chromatin accessibility correlating with differentiation state-specific gene expression

2019 ◽  
Vol 453 (1) ◽  
pp. 86-104 ◽  
Author(s):  
Joshua Disatham ◽  
Daniel Chauss ◽  
Rifah Gheyas ◽  
Lisa Brennan ◽  
David Blanco ◽  
...  
Keyword(s):  
Gene Expression ◽  
Chromatin Accessibility ◽  
Specific Gene ◽  
Specific Gene Expression

p130Cas-dependent actin remodelling regulates myogenic differentiation

2012 ◽  
Vol 445 (3) ◽  
pp. 323-332 ◽  
Author(s):  
Keiko Kawauchi ◽  
Wee Wee Tan ◽  
Keigo Araki ◽  
Farhana Binte Abu Bakar ◽  
Minsoo Kim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Nuclear Localization ◽  
Myogenic Differentiation ◽  
Specific Gene ◽  
Control Of Gene Expression ◽  
Cytoskeletal Organization ◽  
Specific Gene Expression ◽  
Myotube Formation ◽  
Integrin Β3 ◽  
Actin Remodelling

Actin dynamics are implicated in various cellular processes, not only through the regulation of cytoskeletal organization, but also via the control of gene expression. In the present study we show that the Src family kinase substrate p130Cas (Cas is Crk-associated substrate) influences actin remodelling and concomitant muscle-specific gene expression, thereby regulating myogenic differentiation. In C2C12 myoblasts, silencing of p130Cas expression by RNA interference impaired F-actin (filamentous actin) formation and nuclear localization of the SRF (serum-response factor) co-activator MAL (megakaryocytic acute leukaemia) following the induction of myogenic differentiation. Consequently, formation of multinucleated myotubes was abolished. Re-introduction of wild-type p130Cas, but not its phosphorylation-defective mutant, into p130Cas-knockdown myoblasts restored F-actin assembly, MAL nuclear localization and myotube formation. Depletion of the adhesion molecule integrin β3, a key regulator of myogenic differentiation as well as actin cytoskeletal organization, attenuated p130Cas phosphorylation and MAL nuclear localization during C2C12 differentiation. Moreover, knockdown of p130Cas led to the activation of the F-actin-severing protein cofilin. The introduction of a dominant-negative mutant of cofilin into p130Cas-knockdown myoblasts restored muscle-specific gene expression and myotube formation. The results of the present study suggest that p130Cas phosphorylation, mediated by integrin β3, facilitates cofilin inactivation and promotes myogenic differentiation through modulating actin cytoskeleton remodelling.

scholarly journals Accurate transcription start sites enable mining for the cis-regulatory determinants of tissue specific gene expression

2020 ◽  
Author(s):  
Mitra Ansariola ◽  
Valerie N. Fraser ◽  
Sergei A. Filichkin ◽  
Maria G. Ivanchenko ◽  
Zachary A. Bright ◽  
...  
Keyword(s):  
Gene Expression ◽  
Binding Sites ◽  
Chromatin Accessibility ◽  
Specific Gene ◽  
Open Chromatin ◽  
Transcription Start ◽  
Tissue Specific ◽  
Transcription Start Sites ◽  
Tissue Specific Gene ◽  
Specific Gene Expression

AbstractAcross tissues, gene expression is regulated by a combination of determinants, including the binding of transcription factors (TFs), along with other aspects of cellular state. Recent studies emphasize the importance of both genetic and epigenetic states – TF binding sites and binding site chromatin accessibility have emerged as potentially causal determinants of tissue specificity. To investigate the relative contributions of these determinants, we constructed three genome-scale datasets for both root and shoot tissues of the same Arabidopsis thaliana plants: TSS-seq data to identify Transcription Start Sites, OC-seq data to identify regions of Open Chromatin, and RNA-seq data to assess gene expression levels. For genes that are differentially expressed between root and shoot, we constructed a machine learning model predicting tissue of expression from chromatin accessibility and TF binding information upstream of TSS locations. The resulting model was highly accurate (over 90% auROC and auPRC), and our analysis of model contributions (feature weights) strongly suggests that patterns of TF binding sites within ∼500 nt TSS-proximal regions are predominant explainers of tissue of expression in most cases. Thus, in plants, cis-regulatory control of tissue-specific gene expression appears to be primarily determined by TSS-proximal sequences, and rarely by distal enhancer-like accessible chromatin regions. This study highlights the exciting future possibility of a native TF site-based design process for the tissue-specific targeting of plant gene promoters.

scholarly journals Runx2 Is a Common Target of Transforming Growth Factor β1 and Bone Morphogenetic Protein 2, and Cooperation between Runx2 and Smad5 Induces Osteoblast-Specific Gene Expression in the Pluripotent Mesenchymal Precursor Cell Line C2C12

2000 ◽  
Vol 20 (23) ◽  
pp. 8783-8792 ◽  
Author(s):  
Kyeong-Sook Lee ◽  
Hyun-Jung Kim ◽  
Qing-Lin Li ◽  
Xin-Zi Chi ◽  
Chisato Ueta ◽  
...  
Keyword(s):  
Gene Expression ◽  
Transforming Growth Factor ◽  
Myogenic Differentiation ◽  
Transforming Growth Factor Β1 ◽  
C2c12 Cells ◽  
Bone Morphogenetic Protein 2 ◽  
Specific Gene ◽  
Specific Gene Expression ◽  
Morphogenetic Protein ◽  
Tgf Β1

ABSTRACT When C2C12 pluripotent mesenchymal precursor cells are treated with transforming growth factor β1 (TGF-β1), terminal differentiation into myotubes is blocked. Treatment with bone morphogenetic protein 2 (BMP-2) not only blocks myogenic differentiation of C2C12 cells but also induces osteoblast differentiation. The molecular mechanisms governing the ability of TGF-β1 and BMP-2 to both induce ligand-specific responses and inhibit myogenic differentiation are not known. We identified Runx2/PEBP2αA/Cbfa1, a global regulator of osteogenesis, as a major TGF-β1-responsive element binding protein induced by TGF-β1 and BMP-2 in C2C12 cells. Consistent with the observation that Runx2 can be induced by either TGF-β1 or BMP-2, the exogenous expression of Runx2 mediated some of the effects of TGF-β1 and BMP-2 but not osteoblast-specific gene expression. Runx2 mimicked common effects of TGF-β1 and BMP-2 by inducing expression of matrix gene products (for example, collagen and fibronectin), suppressing MyoD expression, and inhibiting myotube formation of C2C12 cells. For osteoblast differentiation, an additional effector, BMP-specific Smad protein, was required. Our results indicate that Runx2 is a major target gene shared by TGF-β and BMP signaling pathways and that the coordinated action of Runx2 and BMP-activated Smads leads to the induction of osteoblast-specific gene expression in C2C12 cells.

scholarly journals TBP/TFIID-dependent activation of MyoD target genes in skeletal muscle cells

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Barbora Malecova ◽  
Alessandra Dall'Agnese ◽  
Luca Madaro ◽  
Sole Gatto ◽  
Paula Coutinho Toto ◽  
...  
Keyword(s):  
Gene Expression ◽  
Target Genes ◽  
Control Cell ◽  
Myoblast Differentiation ◽  
Specific Gene ◽  
Specific Gene Expression ◽  
Muscle Gene Expression ◽  
Primary Mouse ◽  
Muscle Genes ◽  
Muscle Gene

Change in the identity of the components of the transcription pre-initiation complex is proposed to control cell type-specific gene expression. Replacement of the canonical TFIID-TBP complex with TRF3/TBP2 was reported to be required for activation of muscle-gene expression. The lack of a developmental phenotype in TBP2 null mice prompted further analysis to determine whether TBP2 deficiency can compromise adult myogenesis. We show here that TBP2 null mice have an intact regeneration potential upon injury and that TBP2 is not expressed in established C2C12 muscle cell or in primary mouse MuSCs. While TFIID subunits and TBP are downregulated during myoblast differentiation, reduced amounts of these proteins form a complex that is detectable on promoters of muscle genes and is essential for their expression. This evidence demonstrates that TBP2 does not replace TBP during muscle differentiation, as previously proposed, with limiting amounts of TFIID-TBP being required to promote muscle-specific gene expression.

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