Submission Date

7-21-2017

Document Type

Paper- Restricted to Campus Access

Department

Biology

Faculty Mentor

Rebecca Lyczak

Comments

Presented during the 19th Annual Summer Fellows Symposium, July 21, 2017 at Ursinus College.

Supported by a National Institutes of Health Academic Research Enhancement Award (AREA) grant (1 R15 GM110614-01).

Project Description

The anterior-posterior axis in the C. elegans embryo is set up after the first asymmetric cell division creates two differently sized daughter cells. One of the genes involved 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 36%-42%. Previous work located lz5 to chromosome II, identified 14 potential suppressors, and narrowed down these options to two candidate genes. RNA interference (RNAi) and genetic crosses were used to investigate these genes to determine which is lz5. Findings from crosses and RNAi indicate that one of the candidate genes, a dual-specificity protein kinase, is the lz5 suppressor. In the future, these findings will hopefully be used to better understand lz5’s mechanism of suppression and pam-1’s role in embryonic development.

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