Submission Date

7-19-2018

Document Type

Paper- Restricted to Campus Access

Department

Biology

Faculty Mentor

Rebecca Lyczak

Comments

Presented during the 20th Annual Summer Fellows Symposium, July 20, 2018 at Ursinus College.

Supported by a National Institutes of Health Academic Research Enhancement Award (AREA) grant (1R15GM110614-02).

Project Description

C. elegans are self-fertilizing hermaphrodites, meaning they provide both the egg and sperm for their offspring. A missense mutation in a gene of C. elegans, which has a mutation called lz5 (although this study does not investigate the lz5 mutation) which inhibits mitosis promoting factor (MPF) in oocytes (unfertilized eggs) and keeps them from developing prematurely, was found to reduce the effects of a mutation in the pam-1 gene, which is crucial for anterior-posterior axis establishment. In addition to this, the pam-1 mutation protects the worm from the effects of lz5 RNAi (sterility). This study sought to determine the time course it takes for lz5 RNAi to induce sterility in wildtype and pam-1 mutants, and the percentage of worms that actually go sterile. The results show that in wildtype, lz5 RNAi treated worms laid less embryos than worms treated with the control RNAi, and were more likely to induce sterility after 24 hours. However, in pam-1 mutants, lz5 RNAi treated worms laid more embryos than worms treated with the control RNAi, and were not any more likely to induce sterility after 24 hours. Thus it was concluded that lz5 RNAi causes wildtype worms to lay less embryos after 24 hours, but pam-1 mutants are protected from this sterility, in contrast to wildtypes. Thus pam-1 and lz5 genetically interact. This suggests a role for PAM-1 in oocyte maturation.

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