The goal of my project in the Raper Lab is to investigate the genetic interactions between the semaphorin-3fa (sema3fa) and neuropilin-2a (nrp2a) in the context how these genes help organize the olfactory nervous system in zebrafish. Individually, mutations in these genes cause axons to mistarget, or terminate in bundles of neurons (protoglomeruli) that they do not belong. Since these genes are shown to be a receptor-ligand pair in vitro, they may interact within the same biological pathway in vivo in this context. In my project, I create three-day-old embryos containing both of these mutations, and compare them to their siblings containing only one or none of these mutations. If these two genes indeed interact within the same biological pathway, I expect a synergistic addition of effects in embryos that are heterozygous for only one gene as opposed to both, as two small defects in the same pathway compound each other, and no additional effects outside those caused by nrp2a or sema3fa knockouts on their own when both genes are completely knocked out in the pathway in homozygous mutants.
The goal of my project in the Raper Lab is to investigate the genetic interactions between the semaphorin-3fa (sema3fa) and neuropilin-2a (nrp2a) in the context how these genes help organize the olfactory nervous system in zebrafish. Individually, mutations in these genes cause axons to mistarget, or terminate in bundles of neurons (protoglomeruli) that they do not belong. Since these genes are shown to be a receptor-ligand pair in vitro, they may interact within the same biological pathway in vivo in this context. In my project, I create three-day-old embryos containing both of these mutations, and compare them to their siblings containing only one or none of these mutations. If these two genes indeed interact within the same biological pathway, I expect a synergistic addition of effects in embryos that are heterozygous for only one gene as opposed to both, as two small defects in the same pathway compound each other, and no additional effects outside those caused by nrp2a or sema3fa knockouts on their own when both genes are completely knocked out in the pathway in homozygous mutants.