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Possible integration of upstream signals at Cdc42 in filamentous differentiation of S. cerevisiae
Author(s) -
Wu Xiaofeng,
Jiang Yi Wei
Publication year - 2005
Publication title -
yeast
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.923
H-Index - 102
eISSN - 1097-0061
pISSN - 0749-503X
DOI - 10.1002/yea.1294
Subject(s) - biology , microbiology and biotechnology , cdc42 , mitosis , cyclin dependent kinase 1 , sister chromatids , genetics , cell cycle , signal transduction , gene , chromosome
Various environmental stimuli (such as nitrogen starvation, short‐chain alcohols and slowed DNA synthesis) induce filamentous differentiation in S. cerevisiae . Genetic mutations (such as deletion of the mitotic cyclin gene CLB2 ) cause constitutive filamentous differentiation. Although different stimulus‐induced filamentous differentiation involves different signalling pathways, Cdc42 has been identified as a common regulator. We show here that Cdc42 is also required for hydroxyurea (HU)‐induced and clb2 Δ‐caused filamentous growth. We show that the mitotic CDK Clb2/Cdc28 functions upstream of Cdc42 in regulating filamentous differentiation. This result points to possible existence of a Cdc42‐MAPK‐Clb2/Cdc28 positive feedback loop in the signalling of filamentous differentiation. We report isolation of a cdc42‐Y40F allele that blocks HU‐induced, but not nitrogen starvation‐induced, short‐chain alcohol‐induced or clb2 Δ‐caused, filamentation. Based on these results, we propose a model in which Cdc42 functions as a possible integrator for the upstream signals of filamentous differentiation (from the filamentous growth MAPK pathway, the cAMP pathway and the Mec1/Rad53 checkpoint pathway). We also show evidence that the mitotic CDK inhibitor Swe1 may mediate the cross‐talk between the cAMP and MAPK pathways. Copyright © 2005 John Wiley & Sons, Ltd.