Genetic Analysis of Cell Polarity in C. Elegans

Harvard University, Cambridge MA

Investigators

Abstract

0110480 Hunter Genetic analysis of asymmetric cell division in C. elegans early embryos has identified a set of conserved PAR proteins important for the establishment and/or maintenance of zygotic and cellular polarity. The PAR proteins are localized asymmetrically in early blastomeres and their mislocalization correlates with changes in the patterns of cell cleavage and the distribution of cell fate determinants. Drosophila and vertebrate PAR homologs are also asymmetrically localized and important for cell polarity in these animals. Therefore, investigating how the C. elegans PAR proteins become asymmetrically localized and how their activity controls cellular architecture essential for asymmetric cell division is likely to reveal universally important molecular mechanisms. Biochemical analysis in mammalian cells indicates that the highly conserved cell polarity protein Cdc42 binds to and activates the mammalian PAR homologs. Genetic analysis of cdc-42 function in C. elegans early embryos, performed in Dr. Hunter's laboratory, is consistent with these results. Dr. Hunter proposes to investigate how Cdc42 activity controls the localization and activity of the PAR proteins during the establishment of embryonic polarity. A transgenic strain expressing a PAR-6::GFP fusion protein will be constructed and PAR-6:GFP localization followed in living embryos in response to changes in Cdc42 activity. Equally important to how the PAR proteins become asymmetrically localized, is how the PAR proteins control cell polarity. Dr. Hunter proposes a second set of experiments to investigate the function of and determine the molecular identity of roc(qt1), a gene required to coordinate embryonic polarity with cytoskeletal organization.