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« Previous AbstractFus3p and Kss1p control G1 arrest in Saccharomyces cerevisiae through a balance of distinct arrest and proliferative functions that operate in parallel with Far1p    Next AbstractCharacterization of volatile and semi-volatile compounds in green and fermented leaves of Bergenia crassifolia L. by gas chromatography-mass spectrometry and ID-CUBE direct analysis in real time-high resolution mass spectrometry »

Curr Genet


Title:"far4, far5, and far6 define three genes required for efficient activation of MAPKs Fus3 and Kss1 and accumulation of glycogen"
Author(s):Cherkasova V; Elion EA;
Address:"Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, MA 02115, USA. elaine_elion@hms.harvard.edu"
Journal Title:Curr Genet
Year:2001
Volume:40
Issue:1
Page Number:13 - 26
DOI: 10.1007/s002940100217
ISSN/ISBN:0172-8083 (Print) 0172-8083 (Linking)
Abstract:"In Saccharomyces cerevisiae, mating pheromones induce G1 arrest through the activation of two MAP kinases, Fus3 and Kss1. Here we report the isolation of three mutants, far4, far5, and far6, that have the novel phenotype of regulating both the activity of Fus3 and Kss1 and the accumulation of glycogen. A far4 mutation constitutively activates Fus3 and Kss1, reduces glycogen, and blocks G1 arrest in the presence of alpha factor. In contrast, far5 and far6 mutations increase glycogen and reduce activation of Fus3 and Kss1 by pheromone. far4, far5, and far6 are recessive and not allelic to FAR1, FAR3, or 14 genes known to regulate the pheromone response. Non-allelic noncomplementation occurs between far6 and both far4 and far5, suggesting that FAR6 functionally interacts with FAR4 and FAR5. Additional observations suggest that FAR4 has functional overlap with FAR3, which we also find to regulate glycogen accumulation. Our results suggest that the activation of the mating MAPK cascade and subsequent G1 arrest is influenced by a signal transduction pathway that regulates glycogen. In support of this possibility, we find that Fus3 is activated to a greater extent in a 'wimp' strain with defective protein kinase A. Finally, BIM1 and BIK1 have been identified as CEN suppressors of far5, suggesting that the microtubule apparatus may regulate the ability of the pheromone response pathway to promote G1 arrest"
Keywords:"Cell Cycle Proteins/genetics Enzyme Activation Fungal Proteins/*metabolism G1 Phase *Genes, Fungal Genetic Complementation Test Glycogen/metabolism Mating Factor Microtubule Proteins/genetics Mitogen-Activated Protein Kinases/*metabolism Mutation Peptides;"
Notes:"MedlineCherkasova, V Elion, E A eng GM46962/GM/NIGMS NIH HHS/ Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S. 2001/09/26 Curr Genet. 2001 Aug; 40(1):13-26. doi: 10.1007/s002940100217"

 
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