The Yak1 Protein Kinase of Saccharomyces Cerevisiae Moderates Thermotolerance and Inhibits Growth by an Sch9 Protein Kinase-Independent Mechanism
AUTOR(ES)
Hartley, A. D.
RESUMO
The growth defect associated with the loss of yeast A kinase activity can be alleviated by the overexpression or deletion of two other kinases, Sch9 and Yak1, respectively. Using tests of epistasis, we have shown that Sch9 and Yak1 define separate signaling pathways and must, therefore, suppress the A kinase defect by different mechanisms. Nevertheless, the Yak1 kinase appears to regulate cellular processes that are under A kinase control. For example, acquisition of heat resistance is correlated with Yak1 kinase activity, such that YAK1-overexpressing cells are over 200-fold more resistant than isogenic yak1 strains. These results, for the first time, associate a phenotype, other than suppression of the A kinase growth defect, with the loss of Yak1 activity and argue a broader role for the Yak1 kinase in cell growth.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1205801Documentos Relacionados
- PDK1 mediates growth factor-induced Ral-GEF activation by a kinase-independent mechanism
- The Saccharomyces cerevisiae YAK1 gene encodes a protein kinase that is induced by arrest early in the cell cycle.
- KSR stimulates Raf-1 activity in a kinase-independent manner
- Sck1, a High Copy Number Suppressor of Defects in the Camp-Dependent Protein Kinase Pathway in Fission Yeast, Encodes a Protein Homologous to the Saccharomyces Cerevisiae Sch9 Kinase
- Growth factor activation of the estrogen receptor in vascular cells occurs via a mitogen-activated protein kinase-independent pathway.