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A role for cell polarity proteins in mitotic exit
Author(s) -
Höfken Thomas,
Schiebel Elmar
Publication year - 2002
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/cdf481
Subject(s) - mitotic exit , biology , microbiology and biotechnology , mitosis , guanine nucleotide exchange factor , cell polarity , polo like kinase , cdc42 , cytokinesis , anaphase , cell cortex , iqgap1 , gtpase , spindle apparatus , cell division , cell cycle , signal transduction , genetics , cell , cytoskeleton , scaffold protein
The budding yeast mitotic exit network (MEN) is a signal transduction cascade that controls exit from mitosis by facilitating the release of the cell cycle phosphatase Cdc14 from the nucleolus. The G protein Tem1 regulates MEN activity. The Tem1 guanine nucleotide exchange factor (GEF) Lte1 associates with the cortex of the bud and activates the MEN upon the formation of an anaphase spindle. Thus, the cell cortex has an important but ill‐defined role in MEN regulation. Here, we describe a network of conserved cortical cell polarity proteins that have key roles in mitotic exit. The Rho‐like GTPase Cdc42, its GEF Cdc24 and its effector Cla4 [a member of the p21‐activated kinases (PAKs)] control the initial binding and activation of Lte1 to the bud cortex. Moreover, Cdc24, Cdc42 and Ste20, another PAK, probably function parallel to Lte1 in facilitating mitotic exit. Finally, the cell polarity proteins Kel1 and Kel2 are present in complexes with both Lte1 and Tem1, and negatively regulate mitotic exit.