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Calcium regulation of myogenesis by differential calmodulin inhibition of basic helix-loop-helix transcription factors.
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Grundström)
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Grundström)
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Grundström)
2008 (English)In: Molecular Biology of the Cell, ISSN 1059-1524, E-ISSN 1939-4586, Vol. 19, no 6, 2509-2519 p.Article in journal (Refereed) Published
Abstract [en]

The members of the MyoD family of basic helix-loop-helix (bHLH) transcription factors are critical regulators of skeletal muscle differentiation that function as heterodimers with ubiquitously expressed E-protein bHLH transcription factors. These heterodimers must compete successfully with homodimers of E12 and other E-proteins to enable myogenesis. Here, we show that E12 mutants resistant to Ca(2+)-loaded calmodulin (CaM) inhibit MyoD-initiated myogenic conversion of transfected fibroblasts. Ca(2+) channel blockers reduce, and Ca(2+) stimulation increases, transcription by coexpressed MyoD and wild-type E12 but not CaM-resistant mutant E12. Furthermore, CaM-resistant E12 gives lower MyoD binding and higher E12 binding to a MyoD-responsive promoter in vivo and cannot rescue myogenic differentiation that has been inhibited by siRNA against E12 and E47. Our data support the concept that Ca(2+)-loaded CaM enables myogenesis by inhibiting DNA binding of E-protein homodimers, thereby promoting occupancy of myogenic bHLH protein/E-protein heterodimers on promoters of myogenic target genes.

Place, publisher, year, edition, pages
2008. Vol. 19, no 6, 2509-2519 p.
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:umu:diva-20778DOI: 10.1091/mbc.E07-09-0886PubMedID: 18353974OAI: oai:DiVA.org:umu-20778DiVA: diva2:209531
Available from: 2009-03-25 Created: 2009-03-25 Last updated: 2017-12-13Bibliographically approved

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Hauser, JannekSaarikettu, JuhaGrundström, Thomas
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