Presenter: John Flanagan

Faculty Sponsor: Joslyn Mills

School: Bridgewater State University

Research Area: Biochemistry and Molecular Biology

Session: Poster Session 2, 11:30 AM - 12:15 PM, 163, C28

ABSTRACT

The C. elegans protein Lipid-binding protein 3 (LBP-3) is a lipid chaperone which transports polyunsaturated fatty acids (PUFAs) freed by lipolysis of intestinal fat deposits. This lipid signaling pathway involves the interaction of LBP-3 with the nuclear hormone receptor, NHR-49, a process which promotes transcription of life-extending neuropeptides, promoting longevity. A related protein in the nuclear hormone receptor family that could also potentially interact with LBP-3, NHR-86, has been identified as a transcription factor which upregulates immune-related gene expression, drawing question to a potential relationship between lbp-3 and the nematode’s immune response. It is predicted that reduced expression of lbp-3 causes lower levels of NHR-86 activation, impairing the organism’s innate immunity.

To test this hypothesis, physiological, quantitative, and computational experiments were conducted. Physiologically, the effect of reduced lbp-3 expression on the immune system of C. elegans was examined through induced bacterial infection with Bacillus thurgiensis and environmental stress survival assays, including oxidative stress and heat stress. Intestinal permeability was also evaluated to determine the effect of reduced lbp-3expression on localized stress resistance and general integrity of the intestines. To quantify changes in immune-related gene expression, qPCR was conducted, involving genes which are known to be activated by NHR-86. Finally, computational software was used to compare the molecular structures of LBP-3, the lipids which it transports, and the NHR-86 transcription factor to predict sites of chemical interaction.