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Finding Cures. Saving Children.
Kitagawa R: Characterization of CeMAD1–deletion suppressors
In contrast to CeMAD3 which is dispensable, deletion of CeMAD1 is lethal in worms. I have previously isolated and characterized C. elegans strains carrying mutations that suppress the lethality caused by the deletion of the CeMAD1 gene. To elucidate the molecular mechanisms through which these mutations suppress the lethality of worms lacking the SAC, I developed a system to analyze the activity of the anaphase-promoting complex/cyclosome (APC/C) in C. elegans. The APC/C is a large ubiquitn ligase, which targets many proteins for ubiquitn-mediated degradation to promote the metaphase to anaphase transition. I have previously identified a novel protein, IFY-1 as an APC/C substrate in C. elegans. By measuring the amount of IFY-1 in the organisms, I demonstrated that the APC/C activity is increased in most of the CeMAD1-suppressor strains. This finding suggests that mutations that suppress CeMAD1 also affect APC/C activity.
We are collaboratng with Dr. Ann Rose (University of British Columbia, Vancouver, Canada) on this project.
