1996 Fiscal Year Final Research Report Summary
Molecular mechanism of salt tolerance in yeast
| Project/Area Number |
07456050
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
応用微生物学・応用生物化学
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| Research Institution | HIROSHIMA UNIVERSITY |
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Principal Investigator |
MIYAKAWA Tokichi Hiroshima University Faculty of Engineering, Professor, 工学部, 教授 (10116676)
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| Co-Investigator(Kenkyū-buntansha) |
HIRATA Dai Hiroshima University Faculty of Engineering, Assistant Professor, 工学部, 助手 (30243603)
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| Project Period (FY) |
1995 – 1996
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| Keywords | veast / salt tolerance / calcineurin / cation homeostasis |
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| Research Abstract |
We investigated the mechanism for the maintenance of cation homeostasis in the yeast Saccharomyces cerevisiae. Followings are our findings.
1.Salt tolerance mechanism that is regulated by calcineurin and protein kinase A :
W have shown that the expression of ENA1 gene encoding a sodium extrusion pump ATPase which is responsible for decreasing salt concentrations under high salt environmentalconditions, is regulated positively by calcineurin and negatively by protein kinase A.
2.Isolation and characterization of high-salt sensitive mutants :
We isolated 1370 salt sensitive mutants, and classified the mutants to 30 complementation groups. Mutants that were suggested by genetic analysis to be defective in the functions that act downstream of calcineurin were selected (5 complementation groups). Genes that complement the defect of the mutant were isolated. Amongs the genes identified, a gene that encode putative transcription factor was found. The function of this gene in salt tolerance is under investigation.
3.Isolation of muticopy suppressor genes that complement the defect of calcineurin-deficient mutant :
Two each of the genes that encode putative transcription factor and putative membrane transporters were obtained by the screening. The function of these genes is under investigation by gene disruption experiment.
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