This summer, I’m working in the Baugh Lab studying the roundworm Caenorhabditis elegans and the effects of L1 arrest.
C. elegans larvae that hatch into an environment without any nutrients are arrested in the first larval stage of development (L1). This means that they simply do not grow, and they can remain in this stage for weeks. Once they receive enough food, they can resume development as normal.
However, extended L1 arrest can lead to abnormalities in adult C. elegans, just as early-life starvation can cause later problems for humans. Starved worms are more likely to develop issues that interfere with reproduction, including germline tumors and uterine masses. My project investigates potential genetic causes for these abnormalities.
Previous results from my mentor, Ivan, indicate that the C. elegans endogenous RNAi pathway may regulate the abnormalities. RNAi stands for RNA interference, and is a mechanism used to regulate gene expression. Cells recognize double-stranded RNA (often foreign), cut it up, and incorporate it into a protein complex. This complex uses the RNA to recognize specific mRNA molecules, which it binds to and cleaves, preventing them from being translated into proteins. RNAi is used for regulation within the cell and to protect cells against viruses, but is also often leveraged for research, as it can be used to specify and turn off genes.
Right now, I’m primarily looking into genes that code for proteins involved in the RNAi pathway. I’ll be examining the frequency of abnormalities for worms that have certain genes turned off either by mutation or exogenous RNAi. So far, I’ve been maintaining different mutant strains and preparing RNAi, which is delivered to C. elegans through their food. Soon, I’ll be scoring the abnormalities for each strain and RNAi group, and figure out where to go from there!
