| pubmed-article:7050666 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7050666 | lifeskim:mentions | umls-concept:C0036025 | lld:lifeskim |
| pubmed-article:7050666 | lifeskim:mentions | umls-concept:C0031516 | lld:lifeskim |
| pubmed-article:7050666 | lifeskim:mentions | umls-concept:C0596988 | lld:lifeskim |
| pubmed-article:7050666 | lifeskim:mentions | umls-concept:C1517342 | lld:lifeskim |
| pubmed-article:7050666 | lifeskim:mentions | umls-concept:C2003941 | lld:lifeskim |
| pubmed-article:7050666 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
| pubmed-article:7050666 | lifeskim:mentions | umls-concept:C0205463 | lld:lifeskim |
| pubmed-article:7050666 | lifeskim:mentions | umls-concept:C1880022 | lld:lifeskim |
| pubmed-article:7050666 | pubmed:issue | 1 | lld:pubmed |
| pubmed-article:7050666 | pubmed:dateCreated | 1982-10-21 | lld:pubmed |
| pubmed-article:7050666 | pubmed:abstractText | Saccharomyces cerevisiae MATa cells carrying mutations in either sst1 or sst2 are supersensitive to the G1 arrest induced by alpha factor pheromone. When sst1 mutants were mixed with normal SST+ cells, the entire population recovered together from alpha factor arrest, suggesting that SST+ cells helped sst1 mutants to recover. Complementation tests and linkage analysis showed that sst1 and bar1, a mutation which eliminates the ability of MATa cells to act as a "barrier" to the diffusion of alpha factor, were lesions in the same genes. These findings suggest that sst1 mutants, are defective in recovery from alpha factor arrest because they are unable to degrade the pheromone. In contrast, recovery of sst2 mutants was not potentiated by the presence of SST+ cells in mixing experiments. When either normal MATa cells or mutant cells carrying defects in sst1 or sst2 were exposed to alpha factor for 1 h and then washed free of the pheromone, the sst2 cells subsequently remained arrested in the absence of alpha factor for a much longer time than SST+ or sst1 cells. These observations suggest that the defect in sst2 mutants is intrinsic to the cell and is involved in the mechanism of alpha factor action at some step after the initial interaction of the pheromone with the cell. The presence of an sst2 mutation appears to cause a growth debility, since repeated serial subculture of haploid sst2-1 strains led to the accumulation of faster-growing revertants that were pheromone resistant and were mating defective ("sterile"). | lld:pubmed |
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| pubmed-article:7050666 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7050666 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7050666 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7050666 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7050666 | pubmed:month | Jan | lld:pubmed |
| pubmed-article:7050666 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:7050666 | pubmed:author | pubmed-author:ChanR KRK | lld:pubmed |
| pubmed-article:7050666 | pubmed:author | pubmed-author:OtteC ACA | lld:pubmed |
| pubmed-article:7050666 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7050666 | pubmed:volume | 2 | lld:pubmed |
| pubmed-article:7050666 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7050666 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7050666 | pubmed:pagination | 21-9 | lld:pubmed |
| pubmed-article:7050666 | pubmed:dateRevised | 2010-11-18 | lld:pubmed |
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| pubmed-article:7050666 | pubmed:year | 1982 | lld:pubmed |
| pubmed-article:7050666 | pubmed:articleTitle | Physiological characterization of Saccharomyces cerevisiae mutants supersensitive to G1 arrest by a factor and alpha factor pheromones. | lld:pubmed |
| pubmed-article:7050666 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7050666 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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