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dc.contributor.authorDeande, Matthew Thomas
dc.contributor.authorHayashi, Merrick Max
dc.contributor.authorBougoulias, Michael
dc.contributor.authorSmith, Brock David
dc.contributor.authorHilbig, Gabriel
dc.date.accessioned2018-08-06T14:41:33Z
dc.date.available2018-08-06T14:41:33Z
dc.date.copyright2018-05
dc.date.issued2018-08-06
dc.identifier.urihttp://hdl.handle.net/2104/10398
dc.description.abstractWhile many factors show to affect egg laying in C. elegans, we are interested in the downstream effects of Toll-like receptors (TLRs) and their impact on egg laying because a direct relationship is still unknown. Studies have shown the importance of TLRs in the innate immunity of C. elegans and their ability to prevent gram-negative bacterial growth by identification of a single gene for TLR, tol-1. We hypothesize that tol-1 deficient C. elegan mutants will display a reduction in egg laying compared to the wild-type, due to a hindrance in an unknown signal transduction cascade. Part of this pathway would include the C. elegans' response to serotonin, a neurotransmitter stimulating hermaphrodite specific motorneurons (HSN), playing a central role in up-regulation of egg-laying behavior. In this study, egg laying assays were performed on N2 wild-type and tol-1 deficient C. elegans in serotonin. Additionally, the tol-1-/- worms were exposed to EMS mutagenesis, furthering our study. Results show that these worms experienced an increase in egg laying in the F2 generation, overcoming their initial resistance. Further experiments can be performed to elucidate the mechanism by which tol-1 deficient C. elegans overcame this mutation allowing them to surpass the N2 in egg laying ability.en_US
dc.description.sponsorshipDr. Myeongwoo Leeen_US
dc.language.isoen_USen_US
dc.subjectEgg-layingen_US
dc.subjectCaenorhabditis elegansen_US
dc.subjectSerotoninen_US
dc.subjectToll-like receptor (TLR)en_US
dc.titleThe Effect of Mutations in Toll-like Receptors on Caenorhabditis elegans Egg-Laying signalingen_US
dc.typePresentationen_US
dc.rights.accessrightsWorldwide accessen_US
dc.contributor.schoolsBaylor University. Dept. of Biology.en_US


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