| Description |
Neurons comprise the nervous system-the essential signaling and communication system for nearly all multicellular organisms. To coordinate cells across an entire organism, they must grow to be relatively long. Therefore, neurons extend axons from the cell body. Immature neurons extend growth cones at the ends of their axons as they develop, forming synapses.1 Following formation of the synapse, healthy neurons enter a mature state where they cease to extend growth cones, stabilizing the synapse.2 Neurons that never mature continue sprouting growth cones, destabilizing their synapses. The genes kin-20 and unc-119 are required for this transition to maturity, however the mechanisms by which they function remain incompletely understood. The objective of this research was to identify genes in C. elegans which encode proteins that phenotypically suppress kin-20 and unc-119 knockouts to better understand their pathways. The kin-20 and unc-119 knockouts were previously created in a selection for resistance to an acetylcholinesterase inhibitor. Mutations in kin-20 and unc-119 were early stop mutations. In turn, I characterized suppressor mutations, which restored function to these mutants after random mutagenesis followed by selection. Eleven suppressors, including two kin-20(-) and all nine unc-119(-) suppressors, were found to be null revertants-the mutagen reverted the premature stop causing the knockout to a coding mutation. Three kin-20 suppressors were mapped: one to the X chromosome, the gene f13d11.10 is potentially responsible; two were loosely correlated with chromosomes III and X, and the genes madf-8 and h11e01.3 may cause suppression. SNP mapping of a third mutation is ongoing. The purpose of this project was to help in forming a more complete understanding of neuronal maturation, especially axon growth. |
