Study demonstrates Mrtfa regulates actomyosin contractility and junction remodeling during neurulation in Xenopus embryos, indicating essential cellular functions.
Myocardin-related transcription factor A (Mrtfa), also known as megakaryoblastic leukemia protein (Mkl1/MAL), associates with serum response factor (Srf) to regulate transcription in response to actin dynamics, however, the functions of Mrtfa in vertebrate embryos remain largely unknown. Here we show that Mrtfa is required for neural plate folding in early Xenopus embryos. Mrtfa knockdown reduced F-actin levels and inhibited apical constriction in the neural and nonneural ectoderm. By contrast, overexpression of constitutively active Mrtfa induced apical constriction in ectodermal cells via remodeling of tricellular junctions and junctional recruitment of Myosin II. We also identify potential Mrtfa target genes in embryonic ectoderm that encode actins and many regulators of actomyosin networks and junction remodeling. Our findings suggest a role of Mrtfa in the control of morphogenetic movements during neurulation. We propose that the regulation of actomyosin contractility is an essential cellular response to Mrtfa-dependent transcriptional activation.
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