Researcher(s)
- Tyler Vanson, Biological Sciences, University of Delaware
Faculty Mentor(s)
- Aimee Jaramillo-Lambert, Biology, University of Delaware
Abstract
Characterizing the effects of WEE-1 in C. elegans Spermatogenesis
Vanson, T., Pfeiffer, S., Jaramillo-Lambert, A.
Approximately 17.5% of the global population experience infertility because of egg or sperm defects (World Health Organization). Defects in gametic cells can occur when there is an error in the highly regulated process of meiosis. A key component of this regulatory system is the inhibitor protein WEE-1.3, which temporarily prevents the sperm or egg cell’s entry into cell division of meiosis I through its ability to regulate the activation of CDK-1/cyclin-B, the protein complex that allows the gametes to divide. While WEE-1.3 has been well studied in mitotic cell division and the production of eggs, the specific mechanisms of WEE-1.3 in spermatogenesis, sperm formation, is less well known. However, preliminary experiments from the Jaramillo-Lambert Lab with C. elegans reveal that when the protein, WEE-1.3, is depleted through selective degradation from the male germline by auxin-inducible degradation there are subsequent abnormalities in chromosome segregation of meiosis, presumably because of the presence of active CDK-1 complexes without WEE-1.3, allowing for premature entry into meiosis. Through the use of C. elegans strain with a temperature sensitive mutation in cdk-1, I hypothesize that by incubating this strain at a nonpermissive temperature of 25℃ while sperm cells are actively dividing, there will be some degree of restoration in chromosome segregation. Even with WEE-1.3 depletion, increased time to prepare for cell division may counteract these defects. If there is some degree of restoration in chromosome segregation that could suggest that in spermatogenesis WEE-1.3 is the central inhibitor of CDK-1.