We are interested ina the mechanisms controlling embryonic gene expression that result in the differentiation of omnipotent cells into one of several cell fates. Our model system revolves around myogenesis during embryonic development in the nematode C. elegans. Specifically, we have focused on the nematode homologs of genes encoding myogenic regulatory factors known to be critical in vertebrate myogenesis (eg. MyoD, E12/Da, and MEF2). We want to know what role, if any, these homologs play during nematoide myogenesis. The simplicity of the namatode, both in terms of th anatomy and the developmental complexity, allows us to study the expression of these factors in detail. We can also address the function of these genes by inactivating them through mutations. We have shown that, as in mammals, CeMyoDS is required to generate functional muscle during embryogenesis. However, unlike mammals in which the myoD gene family is required for striated muscle determination, C. elegans striated muscle is determined and undergoes substantial differentiation in the absence of CeMyoD. The nematode homologs of both E12/Da and MEF2 also show differences in expression patterns and functions when compared to the vertebrates and Drosophila. Despite the extreme conservation of these factors, from nematodes to humans, the emerging picture is that the developmental processes in which they function are far less conserved.
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