A Number Of PTEN Practices Simplified

4%; n?=?287). In CDK inhibitor contrast, 16.6% of the dyn1�� mutant cells were binucleated (n?= 259), and this fraction rose to 33.2% (n?= 286; p?PTEN 2003, Leisner et?al., 2008?and?Kammerer et?al., 2010). Deletion of DYN1 did not affect the alignment of metaphase spindles (21.7�� �� 1.6��), whereas inactivation of MEN and Nud1 did (30.6�� �� 1.6�� in tem1-3 cells, 31.4�� �� 1.8�� in cdc15-1, 31.6�� �� 1.7�� in dbf2-2 dbf20��, and 36.1�� �� 1.8�� in nud1-44 cells; compared to WT all p?TSA HDAC manufacturer Cdk1-dependent phosphorylation and affects Kar9 distribution ( Liakopoulos et?al., 2003?and?Moore and Miller, 2007). Thus, we investigated whether Nud1 or MEN inactivation also affected the localization of Kar9. Time-lapse movies of 100?s (10 frames) were recorded, and the distribution of Kar9-YFP was scored in wild-type and mutant cells coexpressing CFP-Tub1 ( Figure?3A). All metaphase cells were sorted in either one of the three following classes. ��Strongly asymmetric�� cells carried Kar9 exclusively on one side of the spindle throughout the movie. In ��symmetric�� cells, roughly equal amounts of Kar9 appeared on both sides of the spindle over the course of the movie, and ��weakly asymmetric�� cells showed intermediate Kar9 localization. At 22��C, 81.4% �� 1.7% of wild-type metaphase cells fell in the strongly asymmetric class ( Figure?3B). This value was reduced in dbf2�� and dbf20�� mutant cells (68.2% �� 3.5% and 65.6% �� 8.0%, respectively, p?