Involvement of Nst1p/YNL091w and Msl1p, a U2B'' splicing factor, in Saccharomyces cerevisiae salt tolerance.
Cell tolerance to salt stress depends on many physiological functions, including the best characterized of osmotic adjustment, ion transport and sodium-sensitive sulphate metabolism. From a screening designed to identify novel determinants of salt tolerance we have isolated the YNL091w gene, probably an Ascomycete-specific gene encoding a protein of unknown function. This gene negatively affects salt tolerance and therefore has been designated NST1. The salt tolerance mechanism of nst1 mutants is novel because it is not related to osmoregulation, altered cation accumulation or sulphate metabolism. Genome-wide two-hybrid analysis has suggested that Nst1p interacts with the splicing factor Msl1p and, accordingly, the impact of NST1 on salt tolerance is dependent on a functional MSL1 gene. Loss of MSL1 and NST1 function has pleiotropic phenotypes including increased sensitivity to divalent cations (manganese and zinc) and to caffeine (a cell wall-weakening agent). On the other hand, msl1 mutants but not nst1 mutants are sensitive to thiabendazole (a microtubule-destabilizing agent) and to osmotic stress.[1]References
- Involvement of Nst1p/YNL091w and Msl1p, a U2B'' splicing factor, in Saccharomyces cerevisiae salt tolerance. Goossens, A., Forment, J., Serrano, R. Yeast (2002) [Pubmed]
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