Poster abstracts
Poster number 31 submitted by Kristen Navarro
Characterizing the non-autonomous role of secretory proteins F57B10.5 and C18B12.6 in C. elegans vulval development cell signaling
Kristen Navarro (The Ohio State University, Department of Molecular Genetics)
Abstract:
The Ras protein family is composed of small GTPases that primarily function in cell signaling. When activated, Ras proteins interact with other proteins that will ultimately turn on genes required for cell growth and differentiation. Overactive Ras has been shown to cause cellular overproliferation across multiple eukaryotic species, which may eventually lead to death and disease. In Caenorhabditis elegans (C. elegans) Ras hyperactivity results in a “Multivulva (Muv)” phenotype, resulting in the formation of cell masses in the vulva due to cell hyperproliferation. Previously, a RNAi screen was performed to discover genes that potentially serve as non-autonomous regulators of Ras signaling. In this screen, animals that were RNAi-deficient in all tissues except for the mesoderm were treated with a RNAi genomic library, and screened for phenotype rescue. From the 47 genes found to suppress the mutant phenotype to wild-type, two genes – F57B10.5 and C18B12.6 – were selected for further investigation. These two genes, that encode a transmembrane trafficking protein and endoplasmic reticulum vesicle transporter protein, were selected for further study for their roles in cell secretion. We hypothesize that F57B10.5 and C18B12.6 may regulate Ras signaling by transporting enzymes required to break down the basement membrane between the anchor cell (AC) and P6.p vulval precursor cell. (VPC) This degradation is required for Ras, suggesting that knockdown of F57B10.5 and C18B12.6 may regulate signaling by controlling secretion of proteins that influence the proliferation of cells with overactive Ras. To investigate, we first aim to define the expression pattern of these genes throughout development, define the effects of null mutations in the worm, and investigate if the phenotype suppression present when the genes are knocked down is Ras-specific or not. Next, we will examine how the two genes impact vulval development cell signaling and biology. Finally, we will investigate if these proteins co-localize with each other or other secretion-related proteins, as well as study how knocking down the genes impacts cellular biology. In conclusion, this study aims to investigate how protein secretion and trafficking play a role in cell signaling during development, and how it can serve a regulatory function.
Keywords: Ras, signaling, cell secretion