Involvement of the VDE homing endonuclease and rapamycin in regulation of the Saccharomyces cerevisiae GSH11 gene encoding the high affinity glutathione transporter
Involvement of the VDE homing endonuclease and rapamycin in regulation of the Saccharomyces cerevisiae GSH11 gene encoding the high affinity glutathione transporter
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DOI：
10.1074/jbc.m302084200
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发表时间：
2003-10-10
影响因子：
4.8
通讯作者：
Ono, BI
中科院分区：
文献类型：
--
作者：
Miyake, T;Hiraishi, H;Ono, BI
酿酒酵母基因HGT 1/GSH 11编码高亲和力谷胱甘肽转运蛋白，并被添加到培养基中的半胱氨酸抑制。先前已经发现，5 ′-上游顺式元件CCGCCACAC负责调节GSH 11表达，并且几种蛋白质与该元件结合（Miyake，T.，Kanayama，M.，Sammoto，H.，和小野，B。等人（2002）Mol. Genet. Genomics 266，1004 - 1011）。在这份报告中，我们提出的证据表明，这些蛋白质中最突出的是VDE，以前被称为归巢核酸内切酶编码的VMA 1。我们还表明，GSH 11是不表达的VDE-删除的菌株，不能表达该菌株的GSH 11是克服引入VDE或整个VMA 1基因的编码区。还发现VDE不切割GSH 11顺式元件附近的DNA。雷帕霉素是雷帕霉素靶蛋白（TOR）信号转导系统的抑制剂，在硫饥饿条件下，雷帕霉素以VDE依赖的方式增强GSH 11的表达。这些结果表明，GSH 11是由一个系统敏感的硫饥饿（大概通过半胱氨酸耗尽）和一个更一般的系统，涉及由TOR系统介导的营养饥饿信号的调节。两个系统都需要可操作（抑制TOR和硫饥饿）以完全表达GSH 11。
The Saccharomyces cerevisiae gene HGT1/GSH11 encodes the high affinity glutathione transporter and is repressed by cysteine added to the culture medium. It has been found previously that a 5'-upstream cis-element, CCGCCACAC, is responsible for regulating GSH11 expression and that several proteins bind to this element (Miyake, T., Kanayama, M., Sammoto, H., and Ono, B. (2002) Mol. Genet. Genomics 266, 1004 - 1011). In this report we present evidence that the most prominent of these proteins is VDE, known previously as the homing endonuclease encoded by VMA1. We show also that GSH11 is not expressed in a VDE-deleted strain and that inability to express the GSH11 of this strain is overcome by introduction of the coding region of VDE or the entire VMA1 gene. It is also found that VDE does not cut DNA in the vicinity of the GSH11 cis-element. Rapamycin, an inhibitor of the target of rapamycin (TOR) signal-transduction system, is found to enhance expression of GSH11 in a VDE-dependent manner under conditions of sulfur starvation. These results indicate that GSH11 is regulated by a system sensitive to sulfur starvation ( presumably via cysteine depletion) and a more general system involving the nutritional starvation signal mediated by the TOR system. Both systems need to be operational ( inhibition of TOR and sulfur starvation) for full expression of GSH11.