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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1999-10-20
pubmed:databankReference
pubmed:abstractText
When glucose is added to Saccharomyces cerevisiae cells grown into stationary phase or on non-fermentable carbon sources a rapid loss of heat stress resistance occurs. Mutants that retain high stress resistance after addition of glucose are called 'fil', for deficient in fermentation induced loss of stress resistance. Transformation of the fil1 mutant, which harbours a point mutation in adenylate cyclase, with a yeast gene library on a single copy plasmid resulted in transformants that were again stress-sensitive. One of the genes isolated in this way was a gene of previously unknown function. We have called it SFI1, for suppressor of fil1. SFI1 is an essential gene. Combination of Sfi1 and cAMP pathway mutations indicates that Sfi1 itself is not involved in the cAMP pathway. Conditional sfi1 mutants did not show enhanced heat resistance under the restrictive condition, whereas overexpression of SFI1 rendered cells heat-sensitive. Sfi1 may be a downstream target of the protein kinase A pathway, but its precise relationship with heat resistance remains unclear. Further analysis showed that Sfi1 is required for cell cycle progression, more specifically for progression through G(2)-M transition. Cells expressing SFI1 under the control of a galactose-inducible promoter arrest after addition of glucose as doublets of undivided mother and daughter cells. These doublets contain a single nucleus and lack mitotic spindles. Sfi1 shares homology with Xenopus laevis XCAP-C, a protein required for chromosome assembly. The conserved residues between these two proteins show a strong bias for charged amino acids. Hence, Sfi1 might be required for correct mitotic spindle assembly and its precise role might be in chromosome condensation. In conclusion, we have identified an essential function in the G(2)-M transition of the cell cycle for a yeast gene of previously unknown function.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0749-503X
pubmed:author
pubmed:copyrightInfo
Copyright 1999 John Wiley & Sons, Ltd.
pubmed:issnType
Print
pubmed:volume
15
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1097-109
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:10455233-Base Sequence, pubmed-meshheading:10455233-Cell Cycle Proteins, pubmed-meshheading:10455233-Cloning, Molecular, pubmed-meshheading:10455233-Cyclic AMP, pubmed-meshheading:10455233-DNA, Fungal, pubmed-meshheading:10455233-Flow Cytometry, pubmed-meshheading:10455233-Fluorescent Antibody Technique, Indirect, pubmed-meshheading:10455233-G2 Phase, pubmed-meshheading:10455233-Gene Expression Regulation, Fungal, pubmed-meshheading:10455233-Genes, Fungal, pubmed-meshheading:10455233-Genes, Suppressor, pubmed-meshheading:10455233-Glucose, pubmed-meshheading:10455233-Heat-Shock Response, pubmed-meshheading:10455233-Molecular Sequence Data, pubmed-meshheading:10455233-Mutation, pubmed-meshheading:10455233-Plasmids, pubmed-meshheading:10455233-Recombinant Proteins, pubmed-meshheading:10455233-Repressor Proteins, pubmed-meshheading:10455233-Saccharomyces cerevisiae, pubmed-meshheading:10455233-Saccharomyces cerevisiae Proteins, pubmed-meshheading:10455233-Sequence Analysis, DNA, pubmed-meshheading:10455233-Transformation, Genetic, pubmed-meshheading:10455233-Tubulin, pubmed-meshheading:10455233-ras Proteins
pubmed:year
1999
pubmed:articleTitle
Deletion of SFI1, a novel suppressor of partial Ras-cAMP pathway deficiency in the yeast Saccharomyces cerevisiae, causes G(2) arrest.
pubmed:affiliation
Laboratorium voor Moleculaire Celbiologie, Katholieke Universiteit Leuven, Leuven, Belgium.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't