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MBC in Press, published online ahead of print October 17, 2007
Mol. Biol. Cell 10.1091/mbc.E07-05-0509

A more recent version of this article appeared on December 1, 2007
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Submitted on May 30, 2007
Revised on October 1, 2007
Accepted on October 9, 2007

Identification of Yeast IQGAP (Iqg1p) as an Anaphase-Promoting-Complex Substrate and Its Role in Actomyosin-Ring-Independent Cytokinesis

Nolan Ko,*{dagger} Ryuichi Nishihama,*{dagger} Gregory H. Tully,{ddagger} Denis Ostapenko,{sect} Mark J. Solomon,{sect} David O. Morgan,{ddagger} and John R. Pringle*{dagger}

*Department of Biology, University of North Carolina, Chapel Hill, NC 27599; {dagger}Department of Genetics, Stanford University School of Medicine, Stanford, CA 94305; {ddagger}Department of Physiology, University of California, San Francisco, CA 94143; {sect}Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT 06520

Monitoring Editor: Orna Cohen-Fix

In the yeast S. cerevisiae, a ring of myosin II forms in a septin-dependent manner at the budding site in late G1. This ring remains at the bud neck until the onset of cytokinesis, when actin is recruited to it. The actomyosin ring then contracts, septum formation occurs concurrently, and cytokinesis is soon completed. Deletion of MYO1 (the only myosin II gene) is lethal on rich medium in the W303 strain background and causes slow-growth and delayed-cell-separation phenotypes in the S288C strain background. These phenotypes can be suppressed by deletions of genes encoding nonessential components of the anaphase-promoting complex (APC/C). This suppression does not appear to result simply from a delay in mitotic exit, because overexpression of a nondegradable mitotic cyclin does not suppress the same phenotypes. Overexpression of either IQG1 or CYK3 also suppresses the myo1{Delta} phenotypes, and Iqg1p (an IQGAP protein) is increased in abundance and abnormally persistent after cytokinesis in APC/C mutants. In vitro assays showed that Iqg1p is ubiquitinated directly by APC/CCdh1 via a novel recognition sequence. A nondegradable Iqg1p (lacking this recognition sequence) can suppress the myo1{Delta} phenotypes even when expressed at relatively low levels. Taken together, the data suggest that compromise of APC/C function allows the accumulation of Iqg1p, which then promotes actomyosin-ring-independent cytokinesis at least in part by activation of Cyk3p.

Address correspondence to: John R. Pringle (jpringle{at}stanford.edu)






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