Investigating KLP-20-Dependent miRNA regulation in Caenorhabditis elegans: Mechanisms of neuronal-epidermal cell non-autonomous signaling

Kinesins are microtubule-associated motors essential for intracellular transport, yet their roles in RNA regulation are still not well understood. Our lab previously identified KLP-20 as a novel interactor of the RISC complex (unpublished), with loss of KLP-20 disrupting miRNA-mediated gene silencing. Although KLP-20 expression is restricted to neurons, KLP-20 mutants display characteristic bumpy epidermal phenotype, suggesting a role in neuronal-epidermal communication. We hypothesize that KLP-20 may facilitate the transport of miRNA-RISC complexes from neurons to the epidermis, enabling non-autonomous signaling. Using the nematode C. elegans, we aim to define the role of KLP-20 in miRNA regulation and neuronal to epidermal communication.To address this, I generated numerous RNAi constructs to test candidate genes for suppression of the KLP-20 dependant bumpy epidermal phenotype, expressed miRNAs under an epidermal promoter to assess tissue-specific rescue, and investigated whether KLP-20 mediated miRNA regulation is dependant on miRNA regulatory machinery. This work will advance the understanding of kinesins in miRNA regulation, with implications for neurodegenerative diseases linked to disrupted miRNA pathways.