It is currently unknown if C. elegans with the bbs gene mutation produce any serotonin as they retain their eggs. Egg retention has been linked to low serotonin production within C. elegans. The resulting hypothesis is that C. elegans with the bbs gene mutations lack serotonin. Serotonin reuptake inhibitors or SSRIs are a classification of drugs that increase serotonin levels. We plan on giving SSRIs to a group of C. elegans with the bbs mutation and observe their egg laying capabilities. This presentation will cover the experimental methods of this experiment.

Primary cilia are sensory structures that help cells receive and process signals. When cilia do not function properly, it can lead to human diseases called ciliopathies, including Bardet-Biedl Syndrome (BBS). BBS can cause problems in nearly every system in the body including the nervous system. However, it is not fully understood how defects in ciliary proteins affect neuronal signaling. The gene bbs-5 encodes a protein that is a part of the BBSome complex. This helps regulate protein movement in ciliated cells. In C. elegans, mutations in bbs-5 cause problems in egg laying. Serotonin is a neurotransmitter that controls egg-laying activity, and its production depends on the enzyme TPH-1. It is currently unclear whether the egg laying defects seen in bbs-5 mutants are related to changes in serotonin production and whether these changes could be due to decreased TPH-1 protein levels. Our long-term goal is to better understand how ciliary proteins influence neuronal signals and how this may relate to symptoms seen in ciliopathies. The objective is to determine whether loss of bbs-5 in C. elegans reduces TPH-1 protein levels and has an effect on egg laying which relies on serotonin production. We hypothesize that loss of bbs-5 leads to reduced TPH-1 protein levels, resulting in decreased serotonin production and altered egg laying behavior in C. elegans.