Myogenesis: A View from Drosophila

Memorial Sloan-Kettering Cancer Center, Sloan Kettering Division, Graduate School of Medical Sciences, Cornell University, New York, New York 10021, USA.
Cell (Impact Factor: 33.12). 07/1998; 93(6):921-7. DOI: 10.1016/S0092-8674(00)81198-8
Source: PubMed
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    • "FCs are born from the asymmetric division of progenitor cells (PCs) specified at precise positions and times within the somatic mesoderm. Detailed characterization of a few somatic muscle lineages has established that muscle identity (specific shape, size, orientation) reflects the expression of specific muscle identity transcription factors (iTFs) in each FC that act in a combinatorial manner (Baylies et al., 1998; Frasch, 1999; de Joussineau et al., 2012; Enriquez et al., 2012). "
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    ABSTRACT: The T-box transcription factor Tbx1 and the LIM-homeodomain transcription factor Islet1 are key components in regulatory circuits that generate myogenic and cardiogenic lineage diversity in chordates. We show here that Org-1 and Tup, the Drosophila orthologs of Tbx1 and Islet1, are co-expressed and required for formation of the heart-associated alary muscles (AMs) in the abdomen. The same holds true for lineage-related muscles in the thorax that have not been described previously, which we name thoracic alary-related muscles (TARMs). Lineage analyses identified the progenitor cell for each AM and TARM. Three-dimensional high-resolution analyses indicate that AMs and TARMs connect the exoskeleton to the aorta/heart and to different regions of the midgut, respectively, and surround-specific tracheal branches, pointing to an architectural role in the internal anatomy of the larva. Org-1 controls tup expression in the AM/TARM lineage by direct binding to two regulatory sites within an AM/TARM-specific cis-regulatory module, tupAME. The contributions of Org-1 and Tup to the specification of Drosophila AMs and TARMs provide new insights into the transcriptional control of Drosophila larval muscle diversification and highlight new parallels with gene regulatory networks involved in the specification of cardiopharyngeal mesodermal derivatives in chordates.
    Development 10/2014; 141(19):3761-3771. DOI:10.1242/dev.111005 · 6.27 Impact Factor
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    • "Despite similarities, such as shared expression of contractile proteins, each muscle fiber can be distinguished by properties like its size, shape, orientation, number of nuclei, innervation, and tendon attachment sites (Baylies et al., 1998). Muscle fibers arise by the iterative fusion of two types of myoblasts, called founder cells (FCs) and fusion competent myoblasts (FCMs), to form a syncytium (Rochlin et al., 2010). "
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    ABSTRACT: Skeletal muscles are formed in numerous shapes and sizes, and this diversity impacts function and disease susceptibility. To understand how muscle diversity is generated, we performed gene expression profiling of two muscle subsets from Drosophila embryos. By comparing the transcriptional profiles of these subsets, we identified a core group of founder cell-enriched genes. We screened mutants for muscle defects and identified functions for Sin3A and 10 other transcription and chromatin regulators in the Drosophila embryonic somatic musculature. Sin3A is required for the morphogenesis of a muscle subset, and Sin3A mutants display muscle loss and misattachment. Additionally, misexpression of identity gene transcription factors in Sin3A heterozygous embryos leads to direct transformations of one muscle into another, whereas overexpression of Sin3A results in the reverse transformation. Our data implicate Sin3A as a key buffer controlling muscle responsiveness to transcription factors in the formation of muscle identity, thereby generating tissue diversity.
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    • "Based on mutational analysis, several steps in the myoblast fusion process can be distinguished (Paululat et al., 1999): attraction and adhesion of fusion-competent myoblasts to founder cells (blocked in mbc, sns and Df(1)w 67k30 mutants (Rushton et al., 1995; Bour et al., 2000; Ruiz-Gomez et al., 2000); alignment of fusion-competent myoblasts and founder cells with paired vesicles on either side of the adjoining membranes (the prefusion complex); the formation of electrondense plaques; and, finally, vesiculation and membrane breakdown. For attraction, binding and the initiation of fusion, fusioncompetent myoblasts and founder cells need an asymmetric equipment of extracellular membrane-bound components that allows for attraction and discrimination; fusion-competent myoblasts and founder cells fuse only with cells from the other group, rather than with themselves (Baylies et al., 1998). "
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