Swm1p and
Mnd2p are new components of the budding yeast anaphase-promoting complex.
Andrew M. Page (1),
Vicky Aneliunas, Ben Montpetit, Karen Yuen (1), Christopher Carroll (2), Brian
Snydsman (3), Eric G. Muller, Trisha N. Davis (3), John R. Lamb (4), David O.
Morgan (2), Hieter Philip (1)
(1) CMMT, University of British Columbia, 980 W. 28th Ave., Vancouver, BC
V5Z4H4, Canada (apage@cmmt.ubc.ca); (2) Department of Physiology, University of
California, San Francisco, CA, USA; (3) Department of Biochemistry, University
of Washington, Seattle, WA; (4) Fred Hutchinson Cancer Institute, Seattle, WA,
USA
We identified Swm1p and Mnd2p as multicopy suppressors of cdc23-54 and apc1-21, respectively. swm1 mutants, but not mnd2 mutants, exhibit a temperature sensitive growth defect and delay entry into anaphase. Both Swm1p and Mnd2p co-immunoprecipitate other APC/C components, and both swm1 and mnd2 deletions exhibit genetic interactions with other APC/C components. Deletion of the spindle checkpoint gene MAD2 but not BUB2 partially suppresses the growth defects of swm1. Cells lacking Swm1p, but not Mnd2p, are defective in APC/C substrate turnover in vegetative cells, and in the absence of Swm1p, we observe defects in the integrity of the APC/C complex. Localization studies of fluorescent-tagged APC/C subunits suggest that Apc1p and Swm1p may be sequestered at distinct foci at the nuclear membrane when the APC/C is not active, and redistributed throughout the nucleus at the onset of anaphase. We are currently investigating the localization of APC/C subunits throughout the cell cycle and the contribution of Swm1p and Mnd2p to this process.