Heather Brockway and John MC Ma will Present Their Research July 25, 2013
Heather Brockway’s Abstract:
The Role of the COP9 Signalosome in C. elegans meiosis.
Studies have shown up to 30% of human oocytes are aneuploid and this aneuploidy is the most common cause of birth defects and miscarriages in human reproduction. Research has shown that synaptonemal complex (SC) morphogenesis during meiotic prophase I is critical to proper segregation of chromosomes into gametes and yet, little is known regarding the molecular mechanisms of SC formation and disassembly. The aim of my work is to elucidate the molecular mechanisms of SC morphogenesis and characterize the roles of proteins involved in these pathways. This summer, I plan to examine the role of the COP9/CSN signalosome in meiotic prophase I in the model organism C. elegans. The COP9 signalosome is a key regulator of the ubiquitin degradation pathway and has been shown to interact with several meiotic specific proteins in C. elegans. Mutants in COP9 subunits have defects in meiosis resulting in abnormal gonads. My work indicates a novel role for this complex in SC assembly. I will conduct experiments using genetic, and cell/molecular biology tools to characterize the role of the COP9 complex in meiosis.
John MC Ma’s Abstract:
Substitution of chromosome 17 significantly improves features of the metabolic syndrome in the Lyon hypertensive rat
The Lyon hypertensive rat (LH) is a model for hypertension and several traits of metabolic syndrome, with many of its traits previously found to be associated with rat chromosome (RNO)17. We have been able to generate a consomic rat strain (LH-17LN) by substituting the RNO17 in the LH genome with that of Lyon normotensive (LN), LH’s normotensive control. Phenotyping characterization of LH-17LN demonstrated statistically significant decrease in body length, body weight, adiposity and blood pressure compared to LH. Hence, we conclude RNO17 has statistically significant associations with many features of metabolic syndrome observed in LH. This may be used as a model to further dissect the pathogenesis of hypertension and metabolic syndrome in LH.