Submission Date

4-21-2017

Document Type

Paper- Restricted to Campus Access

Department

Biology

Adviser

Rebecca Lyczak

Committee Member

Rebecca Lyczak

Committee Member

Anthony Lobo

Committee Member

Lisa Grossbauer

Department Chair

Beth Bailey

Project Description

In the nematode Caenorhabditis elegans, cell polarity in the single-cell embryo is indicative of anterior-posterior (AP) axis formation, which is essential for future functional potential. AP axis polarization is initiated by the sperm-donated centrosome contacting the posterior cortex of the embryo resulting in a destabilization of the actomyosin cytoskeleton and eventually polarity establishment. If the centrosome prematurely departs from the posterior cortex, it causes a disruption in PAR protein localization, thus hindering AP axis formation. PAM-1, a puromycin-sensitive aminopeptidase, reinforces two redundant polarization establishment pathways through prolonged centrosome contact with the posterior cortex. pam-1 mutants lack a functional PAM-1 protein, and exhibit a series of abnormalities in polarity landmarks culminating in the failure to properly polarize. Our lab has identified seven suppressor mutations, (lz1-7) of pam-1, which partially rescue the pam-1 phenotype. We have hypothesized that lz4 is a bypass or downstream suppressor of pam-1 and that centrosome dynamics in lz4 strains would resemble wild-type. To establish the relationship of lz4, pam-1 and their targets, I investigated the previously proposed gene identity of lz4, Y48G1C.10, and created a new strain, US127, to investigate lz4 suppression using confocal microscopy. RNAi, and DNA sequencing demonstrated that Y48 was not lz4¸ but I have proposed a new candidate gene, mppa-1, from the same chromosomal region. Analysis of US127 revealed that its centrosome-cortex contact duration was no different from pam-1, and is thus inconsistent with our hypothesis by acting instead through some other mechanism or pathway.

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