Submission Date

7-18-2024

Document Type

Paper- Restricted to Campus Access

Department

Biology

Faculty Mentor

Rebecca Lyczak

Comments

Presented during the 26th Annual Summer Fellows Symposium, July 19, 2024 at Ursinus College.

This research was supported by a grant from the NIH. Grant ID: 2R15GM110614-03

Project Description

Caenorhabditis elegans are transparent nematodes used as model organisms for genetics research as their simple organ systems allow us to make and observe the effect of genetic mutations within the reproductive system to better understand fertility. The puromycin sensitive aminopeptidase PAM-1 is needed to regulate oocyte maturation and oocyte to embryo transition in C. elegans. In wildtype C. elegans a maturation promoting factor (MPF) regulates oocyte maturation. MPF is activated by CDC-25.1, a phosphatase, and is made inactive by WEE-1.3, a kinase. When MPF is active the oocyte matures to be fertilized, and when MPF is inactive oocytes are unable to mature. When wee-1.3 expression is knocked down in wildtype C. elegans, MPF is overactive, and oocyte maturation proceeds too quickly. However, when wee-1.3 expression is knocked down in pam-1 mutants, oocyte maturation is promoted normally, indicating that pam-1 mutations partially protect C. elegans from defects in oocyte maturation. WEE-1.3 is one of many proteins involved in maturation and oocyte to embryo transition. My research looks to address if CDC-25.1 and CDK-1 proteins interact with pam-1 mutants similarly to WEE-1.3, protecting C. elegans from defects in maturation and oocyte to embryo transition. To do so, I will use DIC and confocal microscopy to observe oocyte maturation rates of wildtype and pam-1 mutant C. elegans when the expression of these proteins is knocked down. If interactions are present this would give us a better understanding of the specific role each protein plays in the maturation and development of C. elegans.

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