RNAi pathway components may contribute to starvation-induced gonad abnormalities in Caenorhabditis elegans

Caenorhabditis elegans that hatch into an environment without any nutrients are arrested in the first larval stage of development, L1. Larvae can remain in L1 arrest for weeks and resume normal development once they receive food. However, many C. elegans that experience extended L1 arrest develop abnormal gonads in adulthood, including germ-cell tumors and uterine masses. These growths suggest a misregulation of cell growth. Previous results indicate that genes involved in processing somatic RNA interference (RNAi) could be causing abnormality formation. RNAi refers to a cell’s response to exogenous or endogenous double-stranded RNA. It functions as an internal regulatory mechanism as well as an immune response, allowing sequence-specific suppression of corresponding genes. We hypothesize that endogenous RNAi pathways are involved in the occurrence of starvation-induced gonad abnormalities. It is possible that aberrant small RNAs produced by somatic RNAi machinery are transported to the germline, causing abnormalities to form. We examined rrf-1, ppw-1, rde-1, dcr-1, rde-4, sid-1, alg-1, and rrf-3, which correspond to components of various RNAi pathway branches. Knockout strains and RNAi were used to evaluate the impact of these genes on gonad abnormality frequency in adults following 8 days of L1 arrest. So far, results align with previous findings about somatic RNAi and our transportation hypothesis. We expect future results to further corroborate these findings and clarify the role of different RNAi pathway branches in gonad abnormality formation. Overall, these experiments provide greater insight into the little-known mechanisms regulating pathologies that result from early-life starvation.