Molecular mechanism of salt tolerance in yeast

本文研究了酵母（Saccharomyces cerevisiae）维持阳离子稳态的机制。以下是我们的发现。钙调神经磷酸酶和蛋白激酶A:W调控的耐盐机制表明，在高盐环境条件下，负责降低盐浓度的钠挤压泵atp酶编码的ENA1基因的表达受钙调神经磷酸酶的正调控，而受蛋白激酶A的负调控。高盐敏感突变体的分离和鉴定：我们分离了1370个盐敏感突变体，并将其分类为30个互补组。基因分析表明，在钙调磷酸酶下游的功能上存在缺陷的突变体被选择（5个互补组）。与突变体缺陷互补的基因被分离出来。在鉴定的基因中，发现了一个编码推定转录因子的基因。该基因在耐盐性中的作用正在研究中。对钙调磷酸酶缺陷突变体的多拷贝抑制基因的分离：筛选得到两个编码推定的转录因子和推定的膜转运蛋白的基因。这些基因的功能正在通过基因破坏实验进行研究。

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.