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从酿酒酵母转录活性和非活性基因中诱导去除紫外线诱导的嘧啶二聚体。

Inducible removal of UV-induced pyrimidine dimers from transcriptionally active and inactive genes of Saccharomyces cerevisiae.

作者信息

Waters R, Zhang R, Jones N J

机构信息

School of Biological Sciences, University College of Swansea, UK.

出版信息

Mol Gen Genet. 1993 May;239(1-2):28-32. doi: 10.1007/BF00281597.

Abstract

The prior UV irradiation of alpha haploid Saccharomyces cerevisiae with a UV dose of 25 J/m2 substantially increases the repairability of damage subsequently induced by a UV dose of 70 J/m2 given 1 h after the first irradiation. This enhancement of repair is seen at both the MAT alpha and HML alpha loci, which are, respectively, transcriptionally active and inactive in alpha haploid cells. The presence in the medium of the protein synthesis inhibitor, cycloheximide in the period between the two irradiations eliminated this effect. Enhanced repair still occurred if cycloheximide was present only after the final UV irradiation. This indicated that the first result is not due to cycloheximide merely blocking the synthesis of repair enzymes associated with a hypothetical rapid turnover of such molecules. The enhanced repairability is not the result of changes in chromatin accessibility without protein synthesis, merely caused by the repair of the damage induced by the prior irradiation. The data clearly show that a UV-inducible removal of pyrimidine dimers has occurred which involves the synthesis of new proteins. The genes known to possess inducible promoters, and which are involved in excision are RAD2, RAD7, RAD16 and RAD23. Studies with the rad7 and rad16 mutants which are defective in the ability to repair HML alpha and proficient in the repair of MAT alpha showed that in rad7, preirradiation enhanced the repair at MAT alpha, whereas in rad16 this increased repair of MAT alpha was absent. The preirradiation did not modify the inability to repair HML alpha in either strain. Thus RAD16 has a role in this inducible repair.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

用25 J/m²的紫外线剂量预先照射α单倍体酿酒酵母,会显著提高在首次照射1小时后再给予70 J/m²紫外线剂量所诱导损伤的修复能力。这种修复增强在MATα和HMLα位点均可见,它们在α单倍体细胞中分别处于转录活跃和不活跃状态。在两次照射之间的时间段,培养基中存在蛋白质合成抑制剂环己酰亚胺会消除这种效应。如果环己酰亚胺仅在最终紫外线照射后存在,增强的修复仍会发生。这表明第一个结果并非仅仅是由于环己酰亚胺阻断了与这类分子假设的快速周转相关的修复酶的合成。增强的修复能力不是在没有蛋白质合成的情况下染色质可及性变化的结果,而仅仅是由先前照射诱导的损伤修复所导致。数据清楚地表明发生了紫外线诱导的嘧啶二聚体去除,这涉及新蛋白质的合成。已知具有可诱导启动子且参与切除的基因是RAD2、RAD7、RAD16和RAD23。对rad7和rad16突变体的研究表明,rad7突变体在修复HMLα的能力上有缺陷但能有效修复MATα,rad16突变体则相反,预照射增强了MATα的修复能力,但rad16突变体不存在这种MATα修复增加的情况。预照射并未改变这两种菌株修复HMLα的无能状态。因此,RAD16在这种可诱导修复中起作用。(摘要截断于250字)

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