We are interested in 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 gene encoding CeMyoD, a nematode homolog of the MyoD family of genes that were originally identified as important regulators of myogenesis in the mouse. The simplicity of the nematode, both in terms of the anatomy and the developmental complexity, allows us to study CeMyoD expression in detail. By inactivating the CeMyoD gene through mutation we have shown that, as in mammals, this gene product is required to generate functional muscle during embryogenesis. Animals that lack CeMyoD activity are paralyzed and die shortly after hatching. Because the gene encoding CeMyoD is clearly playing a critical role in determining muscle cell formation, we want to know how the expression of this gene is itself regulated during development. Our analysis of the CeMyoD gene has defined the controlling regions and we are currently attempting to find factors that act through these controlling regions. We have also started to study other regulatory factors that have been shown to be important for myogenesis in other model systems. These include factors such as the heterodimeric partner protein of the MyoD family, called E12, and an unrelated protein called Mef-2.
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