scholarly journals Distinct Protein Arginine Methyltransferases Promote ATP-Dependent Chromatin Remodeling Function at Different Stages of Skeletal Muscle Differentiation

2009 ◽  
Vol 29 (7) ◽  
pp. 1909-1921 ◽  
Author(s):  
Caroline S. Dacwag ◽  
Mark T. Bedford ◽  
Saïd Sif ◽  
Anthony N. Imbalzano
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Chromatin Remodeling ◽  
Muscle Differentiation ◽  
Early Gene ◽  
Late Gene ◽  
Regulatory Sequences ◽  
Skeletal Muscle Differentiation ◽  
Arginine Methyltransferase ◽  
Early Gene Expression

ABSTRACT Temporal regulation of gene expression is a hallmark of cellular differentiation pathways, yet the mechanisms controlling the timing of expression for different classes of differentiation-specific genes are not well understood. We previously demonstrated that the class II arginine methyltransferase Prmt5 was required for skeletal muscle differentiation at the early stages of myogenesis (C. S. Dacwag, Y. Ohkawa, S. Pal, S. Sif, and A. N. Imbalzano, Mol. Cell. Biol. 27:384-394, 2007). Specifically, when Prmt5 levels were reduced, the ATP-dependent SWI/SNF chromatin-remodeling enzymes could not interact with or remodel the promoter of myogenin, an essential early gene. Here we investigated the requirement for Prmt5 and the class I arginine methyltransferase Carm1/Prmt4 in the temporal control of myogenesis. Both arginine methyltransferases could bind to and modify histones at late-gene regulatory sequences. However, the two enzymes showed sequential requirements for gene expression. Prmt5 was required for early-gene expression but dispensable for late-gene expression. Carm1/Prmt4 was required for late- but not for early-gene expression. The reason for the requirement for Carm1/Prmt4 at late genes was to facilitate SWI/SNF chromatin-remodeling enzyme interaction and remodeling at late-gene loci. Thus, distinct arginine methyltransferases are employed at different times of skeletal muscle differentiation for the purpose of facilitating ATP-dependent chromatin-remodeling enzyme interaction and function at myogenic genes.

scholarly journals Calcineurin Broadly Regulates the Initiation of Skeletal Muscle-Specific Gene Expression by Binding Target Promoters and Facilitating the Interaction of the SWI/SNF Chromatin Remodeling Enzyme

2019 ◽  
Vol 39 (19) ◽  
Author(s):  
Hanna Witwicka ◽  
Jumpei Nogami ◽  
Sabriya A. Syed ◽  
Kazumitsu Maehara ◽  
Teresita Padilla-Benavides ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Chromatin Remodeling ◽  
Regulation Of Gene Expression ◽  
Muscle Differentiation ◽  
Specific Gene ◽  
Skeletal Muscle Differentiation ◽  
Promoter Sequences ◽  
Cellular Processes ◽  
Nfat Transcription Factor

ABSTRACT Calcineurin (Cn) is a calcium-activated serine/threonine protein phosphatase that is broadly implicated in diverse cellular processes, including the regulation of gene expression. During skeletal muscle differentiation, Cn activates the nuclear factor of activated T-cell (NFAT) transcription factor but also promotes differentiation by counteracting the negative influences of protein kinase C beta (PKCβ) via dephosphorylation and activation of Brg1, an enzymatic subunit of the mammalian SWI/SNF ATP-dependent chromatin remodeling enzyme. Here we identified four major temporal patterns of Cn-dependent gene expression in differentiating myoblasts and determined that Cn is broadly required for the activation of the myogenic gene expression program. Mechanistically, Cn promotes gene expression through direct binding to myogenic promoter sequences and facilitating the binding of Brg1, other SWI/SNF subunit proteins, and MyoD, a critical lineage determinant for skeletal muscle differentiation. We conclude that the Cn phosphatase directly impacts the expression of myogenic genes by promoting ATP-dependent chromatin remodeling and formation of transcription-competent promoters.

scholarly journals Calcineurin broadly regulates the initiation of skeletal muscle-specific gene expression by binding target promoters and facilitating the interaction of the SWI/SNF chromatin remodeling enzyme

2019 ◽  
Author(s):  
Hanna Witwicka ◽  
Jumpei Nogami ◽  
Sabriya A. Syed ◽  
Kazumitsu Maehara ◽  
Teresita Padilla-Benavides ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Chromatin Remodeling ◽  
Regulation Of Gene Expression ◽  
Muscle Differentiation ◽  
Specific Gene ◽  
Skeletal Muscle Differentiation ◽  
Promoter Sequences ◽  
Cellular Processes ◽  
Nfat Transcription Factor

ABSTRACTCalcineurin (Cn) is a calcium-activated serine/threonine protein phosphatase that is broadly implicated in diverse cellular processes, including the regulation of gene expression. During skeletal muscle differentiation, Cn activates the NFAT transcription factor but also promotes differentiation by counteracting the negative influences of protein kinase C beta (PKCβ) via dephosphorylation and activation of BRG1, an enzymatic subunit of the mammalian SWI/SNF ATP-dependent chromatin remodeling enzyme. Here we identified four major temporal patterns of Cn-dependent gene expression in differentiating myoblasts and determined that Cn is broadly required for the activation of the myogenic gene expression program. Mechanistically, Cn promotes gene expression through direct binding to myogenic promoter sequences and facilitating the binding of BRG1, other SWI/SNF subunit proteins, and MyoD, a critical lineage determinant for skeletal muscle differentiation. We conclude that the Cn phosphatase directly impacts the expression of myogenic genes by promoting ATP-dependent chromatin remodeling and formation of transcription-competent promoters.

scholarly journals Sarcosin (Krp1) in skeletal muscle differentiation: gene expression profiling and knockdown experiments

2012 ◽  
Vol 56 (4) ◽  
pp. 301-309 ◽  
Author(s):  
Leonie Du Puy ◽  
Abdelaziz Beqqali ◽  
Helena T.A. Van Tol ◽  
Jantine Monshouwer-Kloots ◽  
Robert Passier ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Gene Expression Profiling ◽  
Expression Profiling ◽  
Muscle Differentiation ◽  
Skeletal Muscle Differentiation ◽  
Differentiation Gene

scholarly journals MyoD inhibits Fstl1 and Utrn expression by inducing transcription of miR-206

2006 ◽  
Vol 175 (1) ◽  
pp. 77-85 ◽  
Author(s):  
Miriam I. Rosenberg ◽  
Sara A. Georges ◽  
Amy Asawachaicharn ◽  
Erwin Analau ◽  
Stephen J. Tapscott
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Transcriptional Activation ◽  
Cell Types ◽  
Muscle Differentiation ◽  
Skeletal Muscle Differentiation ◽  
Distinct Cell ◽  
Muscle Genes ◽  
Suppression Of Gene Expression ◽  
Dystrophin Protein

Terminal differentiation of distinct cell types requires the transcriptional activation of differentiation-specific genes and the suppression of genes associated with the precursor cell. For example, the expression of utrophin (Utrn) is suppressed during skeletal muscle differentiation, and it is replaced at the sarcolemma by the related dystrophin protein. The MyoD transcription factor directly activates the expression of a large number of skeletal muscle genes, but also suppresses the expression of many genes. To characterize a mechanism of MyoD-mediated suppression of gene expression, we investigated two genes that are suppressed in fibroblasts converted to skeletal muscle by MyoD, follistatin-like 1 (Fstl1) and Utrn. MyoD directly activates the expression of a muscle-specific microRNA (miRNA), miR-206, which targets sequences in the Fstl1 and Utrn RNA, and these sequences are sufficient to suppress gene expression in the presence of miR-206. These findings demonstrate that MyoD, in addition to activating muscle-specific genes, induces miRNAs that repress gene expression during skeletal muscle differentiation.

Early Gene Expression Changes in Skeletal Muscle from SOD1G93A Amyotrophic Lateral Sclerosis Animal Model

2014 ◽  
Vol 34 (3) ◽  
pp. 451-462 ◽  
Author(s):  
Gabriela P. de Oliveira ◽  
Jessica R. Maximino ◽  
Mariana Maschietto ◽  
Edmar Zanoteli ◽  
Renato D. Puga ◽  
...  
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Animal Model ◽  
Amyotrophic Lateral Sclerosis ◽  
Early Gene ◽  
Early Gene Expression ◽  
Lateral Sclerosis

scholarly journals Rearranged JC Virus Noncoding Control Regions Found in Progressive Multifocal Leukoencephalopathy Patient Samples Increase Virus Early Gene Expression and Replication Rate

2010 ◽  
Vol 84 (20) ◽  
pp. 10448-10456 ◽  
Author(s):  
Rainer Gosert ◽  
Piotr Kardas ◽  
Eugene O. Major ◽  
Hans H. Hirsch
Keyword(s):  
Gene Expression ◽  
Progressive Multifocal Leukoencephalopathy ◽  
Simian Virus 40 ◽  
T Antigen ◽  
Early Gene ◽  
Late Gene ◽  
Strong Increase ◽  
Early Gene Expression ◽  
Progressive Multifocal Leukoencephalopathy Patient ◽  
Hiv Aids

ABSTRACT Polyomavirus JC (JCV) infects ∼60% of the general population, followed by asymptomatic urinary shedding in ∼20%. In patients with pronounced immunodeficiency, including HIV/AIDS, JCV can cause progressive multifocal leukoencephalopathy (PML), a devastating brain disease of high mortality. While JCV in the urine of healthy people has a linear noncoding control region called the archetype NCCR (at-NCCR), JCV in brain and cerebrospinal fluid (CSF) of PML patients bear rearranged NCCRs (rr-NCCRs). Although JCV NCCR rearrangements are deemed pathognomonic for PML, their role as a viral determinant is unclear. We sequenced JCV NCCRs found in CSF of eight HIV/AIDS patients newly diagnosed with PML and analyzed their effect on early and late gene expression using a bidirectional reporter vector recapitulating the circular polyomavirus early and late gene organization. The rr-NCCR sequences were highly diverse, but all increased viral early reporter gene expression in progenitor-derived astrocytes, glia-derived cells, and human kidney compared to the expression levels with the at-NCCR. The expression of simian virus 40 (SV40) large T antigen or HIV Tat expression in trans was associated with a strong increase of at-NCCR-controlled early gene expression, while rr-NCCRs were less responsive. The insertion of rr-NCCRs into the JCV genome backbone revealed higher viral replication rates for rr-NCCR compared to those of the at-NCCR JCV in human progenitor-derived astrocytes or glia cells, which was abrogated in SV40 large T-expressing COS-7 cells. We conclude that naturally occurring JCV rr-NCCR variants from PML patients confer increased early gene expression and higher replication rates compared to those of at-NCCR JCV and thereby increase cytopathology.

Induction of cardiac muscle differentiation in isolated animal pole explants of Xenopus laevis embryos

Development ◽  
1993 ◽  
Vol 118 (3) ◽  
pp. 865-875 ◽  
Author(s):  
M. Logan ◽  
T. Mohun
Keyword(s):  
Gene Expression ◽  
Skeletal Muscle ◽  
Growth Factor ◽  
Xenopus Laevis ◽  
Cardiac Muscle ◽  
Muscle Differentiation ◽  
Specific Marker ◽  
Skeletal Muscle Differentiation ◽  
Animal Pole ◽  
Alpha Gene

We have isolated a cDNA fragment encoding a portion of the myosin heavy chain alpha-isoform (XMHC alpha) in the amphibian, Xenopus laevis. The XMHC alpha transcript is highly enriched in adult heart RNA and is expressed exclusively in embryonic heart tissue. It therefore provides a tissue-specific marker for cardiac muscle differentiation during early embryogenesis. Using an RNAase protection assay, we can detect the onset of cardiac muscle differentiation in an anterior, ventral region of tailbud embryos, many hours before the appearance of a beating heart. Whole-mount in situ RNA hybridisation indicates that expression of the XMHC alpha gene is restricted to the developing heart primordium. XMHC alpha gene expression can also be induced in isolated animal pole explants of blastulae by treatment with the growth factor, activin A. Induction is dose-dependent, requiring high doses of the growth factor compared with that required for myotomal (skeletal) muscle differentiation. In contrast, no XMHC alpha transcripts are detected in explants incubated with basic FGF, despite the induction of myotomal muscle differentiation. Activin-induced explants show a similar temporal pattern of XMHC alpha gene expression to that found in normal embryogenesis. Furthermore, cells expressing this gene appear clustered in one or two foci within fused explant aggregates, which often show regular, spontaneous contractions after several days in culture. These results show that terminal differentiation of cardiac muscle can occur in growth factor-induced explants and may be distinguished from skeletal muscle differentiation by the dose and nature of the inducing factor.

Sign in / Sign up

Export Citation Format

Share Document