Friday, October 12, 2012: 10:00 PM
Hall 4E/F (WSCC)
Our laboratory studies cell signaling events related to cell migration, including neuronal axon outgrowth processes. We have chosen the nematode, Caenorhabditis elegans, as our model organism. This roundworm has been extensively genetically manipulated to establish relationships between signaling proteins and resulting whole animal phenotypes. We are interested in C. elegans migration-10 (Mig-10) mutant strains due to Mig-10’s involvement in axonal outgrowth and proper worm development. Mig-10 truncation C. elegans worms demonstrate uncoordinated movement, misplacement of the vulva and excretory canal, and egg-laying-defective phenotypes. In these studies we have injected a DNA construct encoding the wild-type Mig-10 protein into the syncytial gonad of the worm, and hypothesize resultant Mig-10 protein production will rescue the defective phenotype in subsequent progeny. Ultimately, these studies will lead to a better understanding of Mig-10 protein function. This project is supported by the National Institute of Health (NIH), grant number: R25 GM048998-13.