Résumé :
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The myocyte enhancer factor 2 (MEF2) family of MADS (MCMI, agamous, deficiens, serum response factor)-box transcription factors has four members in vertebrates, MEF2A, -B, -C and –D. The four MEF2 genes are expressed in complex and overlapping patterns in embryonic and adult tissues. MEF2 family members have been shown to play a pivotal role in morphogenesis and myogenesis of skeletal, cardiac and smooth muscles cells differentiation and also regulates neuronal and immune cell differentiation. In mice, two unanticipated roles for MEF2C have been recently identified showing that MEF2C controls both chondrocyte hypertrophy and bone development and that the expression of MEF2C in the neural crest is required for craniofacial development. In this study, we describe the cloning of multiple Xenopus MEF2 splicing isoforms differentially expressed during development and show that the accumulation of XMEF2C mRNA was initially specifically located in forming and migrating neural crest. In the tadpole stages, XMEF2C expression was restricted to intersomitic regions and to the peripheral edges of epaxial and cranial muscle masses and was coexpressed with scleraxis, a specific marker for tendons and ligaments. We show that overexpression of XMEF2C inhibited myogenesis, whereas the use of an hormone-inducive MEF2C construct is able to induce scleraxis expression. Furthermore, XMEF2C and scleraxis act cooperatively to induce betaig-h3, a gene expressed in collagen-rich tissues. These findings highlight a previously unappreciated role for XMEF2C in the regulation of tendon development and identify a novel gene transactivation pathway where XMEF2C enhance the ability of the bHLH protein, scleraxis, to activate specific gene expression.
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