Marchler G, Schüller C, Adam G, Ruis H
Institut für Biochemie und Molekulare Zellbiologie, Universität Wien, Austria.
EMBO J. 1993 May;12(5):1997-2003. doi: 10.1002/j.1460-2075.1993.tb05849.x.
Transcription of the Saccharomyces cerevisiae CTT1 gene encoding the cytosolic catalase T is activated by a variety of stress conditions: it is derepressed by nitrogen starvation and induced by heat shock. Furthermore, it is activated by osmotic and oxidative stress. This study shows that a CTT1 upstream region previously found to be involved in nitrogen, cAMP and heat control (base pairs -382 to -325) contains a UAS element (STRE, -368 to -356), which is sufficient for the activation of a reporter gene by all types of stress acting on CTT1. Gel retardation experiments demonstrated the existence of a factor specifically binding to STRE, but to a lesser extent to mutated elements having partly or entirely lost the ability to mediate stress control. Heat activation of STRE, but not of a canonical heat shock element, is enhanced by a ras2 defect mutation, which enhances thermotolerance, and is dramatically reduced by a bcy1 disruption mutation, which decreases thermotolerance. It can be hypothesized, therefore, that the novel stress control element is important for the establishment of induced stress tolerance.
编码胞质过氧化氢酶T的酿酒酵母CTT1基因的转录受多种应激条件激活：氮饥饿可使其去阻遏，热激可诱导其表达。此外，渗透应激和氧化应激也可激活该基因。本研究表明，先前发现参与氮、cAMP和热调控的CTT1上游区域（碱基对-382至-325）包含一个上游激活序列元件（STRE，-368至-356），该元件足以被作用于CTT1的所有类型应激激活报告基因。凝胶阻滞实验证明存在一种特异性结合STRE的因子，但与部分或完全丧失介导应激调控能力的突变元件结合程度较低。ras2缺陷突变可增强耐热性，该突变可增强STRE的热激活，但不增强典型热激元件的热激活；而bcy1缺失突变可降低耐热性，该突变可显著降低STRE的热激活。因此，可以推测，这种新型应激调控元件对于诱导应激耐受性的建立很重要。
