A Study of the Mechanism by which Nicotinamide and TRPV Channels Induce an Egg-Laying Defect in C. elegans
Open Access
Author:
Ido, Liyana Jendre
Millennium Scholars Program:
Biochemistry and Molecular Biology (B M B)
Degree:
Bachelor of Science
Document Type:
Thesis
Thesis Supervisor:
Wendy Hanna-Rose, Thesis Supervisor Charles Fisher, Thesis Supervisor
Keywords:
C. elegans TRPV channel nicotinamide
Abstract:
Nicotinamide (NAM) is known to bind to heterotetrameric TRPV cation channels and cause them to be constitutively active. The OCR-4 and OSM-9 monomers of these channels are necessary for nicotinamide to induce uv-1 cell necrosis and an egg-laying defect (Egl) in which the animal cannot lay eggs. So, while NAM treatment induces these phenotypes in wild-type C. elegans, it induces very little or none of them in osm-9 and ocr-4 mutants lacking TRPV channels. While the cell necrosis and Egl phenotypes are always present or absent together in NAM-treated animals, we know that neither OLQ nor uv-1 cell necrosis causes Egl. I investigate this hypothesis by first inducing the Egl phenotype shown previously in my laboratory’s research. To establish that NAM induces Egl in N2 wild-type worms but not osm-9 worms, I did bagging assays on both strains treated with NAM. I have tested NAM age, NAM time on the plate, NAM concentration, and wild-type strain as causes for the inconsistent Egl phenotype. Thus far, NAM has induced Egl in only about half of wild-type animals regardless of concentration, and only 5.56% Egl in osm-9 animals.
