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首页> 外文期刊>Molecular and Cellular Biology >Regulation of cation transport in Saccharomyces cerevisiae by the salt tolerance gene HAL3.
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Regulation of cation transport in Saccharomyces cerevisiae by the salt tolerance gene HAL3.

机译：耐盐基因HAL3对酿酒酵母中阳离子运输的调节。

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Dynamic regulation of ion transport is essential for homeostasis as cells confront changes in their environment. The gene HAL3 encodes a novel component of this regulatory circuit in the yeast Saccharomyces cerevisiae. Overexpression of HAL3 improves growth of wild-type cells exposed to toxic concentrations of sodium and lithium and suppresses the salt sensitivity conferred by mutation of the calcium-dependent protein phosphatase calcineurin. Null mutants of HAL3 display salt sensitivity. The sequence of HAL3 gives little clue to its function. However, alterations in intracellular cation concentrations associated with changes in HAL3 expression suggest that HAL3 activity may directly increase cytoplasmic K+ and decrease Na+ and Li+. Cation efflux in S. cerevisiae is mediated by the P-type ATPase encoded by the ENA1/PMR24 gene, a putative plasma membrane Na+ pump whose expression is salt induced. Acting in concert with calcineurin, HAL3 is necessary for full activation of ENA1 expression. This functional complementarity is also reflected in the participation of both proteins in recovery from alpha-factor-induced growth arrest. Recently, HAL3 was isolated as a gene (named SIS2) which when overexpressed partially relieves loss of transcription of G1 cyclins in mutants lacking the protein phosphatase Sit4p. Therefore, HAL3 influences cell cycle control and ion homeostasis, acting in parallel to the protein phosphatases Sit4p and calcineurin.
机译：离子迁移的动态调节对于动态平衡至关重要，因为细胞面临着环境变化的挑战。 HAL3基因编码了酿酒酵母中该调节电路的新成分。 HAL3的过表达改善了暴露于钠和锂的有毒浓度的野生型细胞的生长，并抑制了钙依赖性蛋白磷酸酶钙调磷酸酶的突变所赋予的盐敏感性。 HAL3的空突变体显示出盐敏感性。 HAL3的序列对其功能几乎没有提示。但是，与HAL3表达变化相关的细胞内阳离子浓度的变化表明HAL3活性可能直接增加细胞质K +并降低Na +和Li +。酿酒酵母中的阳离子流出是由ENA1 / PMR24基因编码的P型ATPase介导的，该基因是盐诱导的假定质膜Na +泵。 HAL3与钙调神经磷酸酶协同作用，对于ENA1表达的完全激活是必需的。这种功能上的互补性还反映在两种蛋白质参与从α因子诱导的生长停滞中的恢复中。最近，HAL3被分离为一个基因（命名为SIS2），当该基因过度表达时，它可以部分缓解缺少蛋白磷酸酶Sit4p的突变体中G1细胞周期蛋白的转录损失。因此，HAL3与蛋白质磷酸酶Sit4p和钙调神经磷酸酶平行作用，影响细胞周期控制和离子稳态。

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