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Transcription profiling of human skeletal myoblasts misexpressing myocardin

ABSTRACT: transcriptional effects of mis-expression of full length (935) myocardin in growing human skeletal myoblasts Experiment Overall Design: Compare transcriptional profiles of Ad-myocardin infected SKM5 cells with that of Ad-B-gal infected cells

ORGANISM(S): Homo sapiens

SUBMITTER: G Teg Pipes

PROVIDER: E-GEOD-3378 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Stem cells and their derivatives can bypass the requirement of myocardin for smooth muscle gene expression.

Pipes G C Teg GC Sinha Sanjay S Qi Xiaoxia X Zhu Chun-Hong CH Gallardo Teresa D TD Shelton John J Creemers Esther E EE Sutherland Lillian L Richardson James A JA Garry Daniel J DJ Wright Woodring E WE Owens Gary K GK Olson Eric N EN

Developmental biology 20051123 2

The Serum Response Factor (SRF) coactivator myocardin stimulates the transcription of multiple muscle genes during cardiac and smooth muscle development. Mouse embryos lacking myocardin die during the earliest stages of smooth muscle development and fail to express multiple smooth muscle marker genes in the embryonic dorsal aorta and other vascular structures. In this study, we used mutant embryonic stem cell lines to further define the role of myocardin in smooth muscle differentiation and vasc ...[more]

PMID: 16310178

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Effect of myocardin mis-expression in human skeletal myoblasts

Project description:transcriptional effects of mis-expression of full length (935) myocardin in growing human skeletal myoblasts Keywords: mis-expression of transcriptional co-activator

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Project description:Myocardin-related transcription factors (MRTFs) play a central role in the regulation of actin expression and cytoskeletal dynamics. Stimuli that promote actin polymerization allow for shuttling of MRTFs to the nucleus where they activate serum response factor (SRF), a regulator of actin and other cytoskeletal protein genes. SRF is an essential regulator of skeletal muscle differentiation and numerous components of the muscle sarcomere, but the potential involvement of MRTFs in skeletal muscle development has not been examined. We explored the role of MRTFs in muscle development in vivo by generating mutant mice harboring a skeletal muscle-specific deletion of MRTF-B and a global deletion of MRTF-A. These double knockout (dKO) mice were able to form sarcomeres during embryogenesis. However, the sarcomeres were abnormally small and disorganized, causing skeletal muscle hypoplasia and perinatal lethality. Transcriptome analysis demonstrated dramatic dysregulation of actin genes in MRTF dKO mice, highlighting the importance of MRTFs in actin cycling and myofibrillogenesis. MRTFs were also necessary for the survival of skeletal myoblasts and for the efficient formation of intact myotubes. Our findings reveal a central role for MRTFs in sarcomere formation during skeletal muscle development and point to the potential involvement of these transcriptional coactivators in skeletal myopathies. Gene expression profile was generated comparing wild type (WT) and HSA-Cre, MRTF-A/B double knockout mice, by deep seqencing, with three biological replicates, using Illumina HiSeq 2500.

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Homo sapiens

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