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J. Cell. Sci. Jul (2007); 120:2390-401
Rot1 plays an antagonistic role to Clb2 in actin cytoskeleton dynamics throughout the cell cycle-
Juanes MA, Queralt E, Bano MC, Igual JC
Departament de Bioquimica i Biologia Molecular, Facultat de Ciencies Biologiques, Universitat de Valencia, 46100 Burjassot -Valencia-, Spain-
Abstract: ROT1 is an essential gene whose inactivation causes defects in cell cycle progression and morphogenesis in budding yeast- Rot1 affects the actin cytoskeleton during the cell cycle at two levels- First, it is required for the maintenance of apical growth during bud growth- Second, Rot1 is necessary to polarize actin cytoskeleton to the neck region at the end of mitosis; because of this defect, rot1 cells do not properly form a septum to complete cell division- The inability to polarize the actin cytoskeleton at the end of mitosis is not due to a defect in the recruitment of the polarisome scaffold protein Spa2 or the actin cytoskeleton regulators Cdc42 and Cdc24 in the neck region- Previous results indicate a connection between Rot1 and the cyclin Clb2- In fact, overexpression of CLB2 is toxic when ROT1 is partially inactivated, and reciprocally, deletion of CLB2 suppresses the lethality of the rot1 mutant, which indicates a functional antagonism between Clb2 and Rot1- Several genetic interactions suggest a link between Rot1 and the ubiquitin-proteasome system and we show that the Clb2 cyclin is not properly degraded in rot1 cells-
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Chris Stark, Bobby-Joe Breitkreutz, Teresa Reguly, Lorrie Boucher, Ashton Breitkreutz, Mike Tyers.
Nucleic Acids Res. Jan 1;34:D535-9.