FUS3 represses CLN1 and CLN2 and in concert with KSS1 promotes signal transduction

FUS3 is functionally redundant with KSS1, a homologous yeast protein kinase, for a step(s) in signal transduction between the P subunit of the guanine nucleotide binding protein (G protein), STE4, and the mating type-specific transcriptional activator, STE12. Either FUS3 or KSS1 can execute this fun...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 1991-11, Vol.88 (21), p.9392-9396
Main Authors: Elion, E.A. (Massachusetts Institute of Technology, Cambridge, MA), Brill, J.A, Fink, G.R
Format: Article
Language:English
Subjects:
ACCOUPLEMENT
Alleles
Biological and medical sciences
Cell Cycle
Cell cycle, cell proliferation
Cell physiology
COPULA
Cyclins
Fundamental and applied biological sciences. Psychology
Fungal Proteins - metabolism
Genes
GENETICA
GENETIQUE
GTP-Binding Proteins - physiology
LEVADURA
LEVURE
Mating Factor
MEDIO DE CULTIVO
Messenger RNA
MILIEU DE CULTURE
Molecular and cellular biology
MUTACION
MUTATION
Nitrogen
Peptides - metabolism
Pheromones
PLASMIDE
PLASMIDIOS
Plasmids
Protein Kinases - physiology
PROTEINA QUINASA
PROTEINAS
PROTEINE
PROTEINE KINASE
Repression
SACCHAROMYCES CEREVISIAE
Saccharomyces cerevisiae - physiology
Signal Transduction
Time Factors
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Summary:FUS3 is functionally redundant with KSS1, a homologous yeast protein kinase, for a step(s) in signal transduction between the P subunit of the guanine nucleotide binding protein (G protein), STE4, and the mating type-specific transcriptional activator, STE12. Either FUS3 or KSS1 can execute this function; when neither gene encoding these protein kinases is present, signal transduction is blocked, causing sterility. This functional redundancy is strain dependent; some standard laboratory strains (S288C) are kss1-. FUS3 has additional functions required for cell cycle arrest and vegetative growth that do not overlap with KSS1 functions. FUS3 mediates cell cycle arrest during mating through transcriptional repression of two G1 cyclins (CLN1 and CLN2) and through posttranscriptional inhibition of a third G1 cyclin (CLN3). FUS3 is also required for vegetative growth in haploid strains dependent upon CLN3 for cell cycle progression but is not required in strains dependent upon either CLN1 or CLN2, suggesting a functional divergence among the three G1 cyclins. The diverse roles for FUS3 suggest that the FUS3 protein kinase has multiple substrates, some of which may be shared with KSS1
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.88.21.9392