Submission Date

4-23-2018

Document Type

Paper- Restricted to Campus Access

Department

Biology

Adviser

Rebecca Lyczak

Committee Member

Rebecca Lyczak

Committee Member

Anthony Lobo

Committee Member

Jennifer Fleeger

Department Chair

Beth Bailey

Project Description

The anterior-posterior axis in the C. elegans embryo is set up in the one-cell embryo stage and results in an asymmetric cell division, creating two differently sized daughter cells. One of the genes involved in axis establishment is pam-1, which codes for a puromycin-sensitive aminopeptidase. Mutations in this gene cause a symmetric first cell division and a failure to establish the anterior-posterior axis, which leads to high embryonic lethality. Several suppressors of pam-1, which partially rescue the mutant phenotype, have been identified. One of these suppressors, lz5, raises the hatch rate from less than 5% to approximately 40%. Previously in our lab, lz5 was located to chromosome II. Fourteen potential suppressors were identified in this region. We used RNA interference (RNAi) and genetic crosses to investigate these genes and determine a potential candidate gene for lz5, which contains a missense mutation in the suppressed strain. Not only does the candidate gene suppress pam-1 embryonic lethality, but pam-1 protects against additional phenotypes. Wild-type worms treated with RNAi to shut down protein production of this candidate go sterile, but pam-1 mutants do not. Investigation of oocyte maturity markers confirmed that loss of candidate gene expression causes precocious oocyte maturation, but the pam-1 mutation prevents this phenotype and gonads appear wild-type. Thus, we show that these genes genetically interact in both oocyte maturation and embryonic development. This research provides a starting point for continued research into the roles of PAM-1 in C. elegans polarity establishment and cell cycle regulation.

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