Investigating the Molecular Motor Responsible for erm-1 Localization in C. elegans
Karissa Coleman
Cells transport RNA from their nucleus to different target areas within the cell as a form of post-transcriptional gene expression. This mechanism can impact gene expression by either accumulating a desired protein in a specific area of the cell or even targeting mRNA for degradation. Maternally loaded erm-1 transcripts localize to the plasma membrane during the early stages of Caenorhabditis elegans development. The localization of erm-1 mRNA to the plasma membrane has been shown to be guided by its nascent, encoded peptide, similar to the secretory pathway to the Endoplasmic Reticulum (ER). We hypothesize that the mechanism for mRNA transport to membranes is dependent on molecular motors, similar to transport to the ER. Our preliminary data shows that erm-1 mRNA transport is microtubule-dependent. Here, we explore whether dynein, a microtubule motor protein, is required for erm-1 mRNA localization by disrupting dynein through RNA interference (RNAi) followed by imaging erm-1 mRNA by single molecule fluorescence in situ hybridization (smFISH). To ensure the efficacy of the dynein knockdown by RNAi, I employed an embryonic lethality assay to quantify the efficacy of the dynein knockdown. The findings suggest the RNAi treatment was successful at disrupting dynein. Using this result, we can determine whether erm-1 mRNA localization to the plasma membrane is dependent on the molecular motor dynein. ERM proteins are highly conserved in many organisms, and impaired mRNA localization in neurons and other cell types causes disease; therefore, the pathways involved in this mechanism have potential to be generalized to other models.
Dr. Erin Osborne Nishimura
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