Embryonic Morphogenesis: Identifying the Genes Required for C. elegans Gastrulation

Morphogenesis is a collection of processes that organize cells into ordered forms and structures, such as tissues and organs.  A major hurdle in the study of morphogenesis is the redundancy of protein function.  Morphogenesis genes have not fallen out of standard mutagenesis screens in diverse organisms as often as one might anticipate, possibly because of redundancy in genetic pathways for morphogenesis.  Caenorhabditis elegans is an excellent model system to resolve problems of redundancy.  Several techniques allow one to disrupt the function of multiple genes.  For instance, individual genes can be systemically knocked down by the feeding of bacteria expressing dsRNAs targeting genes of choice in genetically null backgrounds.  Alternatively, dsRNA injection into adults can disrupt the functions of several genes simultaneously.

C. elegans gastrulation is the first process of morphogenesis in the developing embryo and begins with the internalization of the two endoderm precursor cells, Ea and Ep.  Traditional mutagenesis screens in C. elegans have identified few genes necessary for gastrulation, presumably due to genetic redundancy.  I have conducted an RNAi feeding screen of candidate genes and have identified cell motility, adhesion, and cytoskeleton proteins with minor roles in gastrulation.  I am pooling these candidate genes and conducting a screen for redundant players by RNAi injection, in hopes of bypassing the obstacle of redundancy to identify proteins that function during C. elegans gastrulation.