Tuite M F, Cox B S
Department of Biological Chemistry, California College of Medicine, University of California, Irvine.
Mol Cell Biol. 1981 Feb;1(2):153-7. doi: 10.1128/mcb.1.2.153-157.1981.
The response of two mutant alleles of the RAD6+ gene of Saccharomyces cerevisiae to the ochre translational suppressor SUQ5 was determined. Both the ultraviolet sensitivity phenotype and the deficiency in ultraviolet-induced mutagenesis phenotype of the rad6-1 allele were suppressed in a [psi+] background. For the rad6-3 allele, only the ultraviolet-sensitivity phenotype was suppressible in a [psi+] background. An SUQ5 rad6-3 [psi+] strain that was examined showed the normal rad6-3 deficiency in ultraviolet-induced mutagenesis. We propose that the RAD6+ gene is divided into two cistrons, RAD6A and RAD6B. RAD6A codes for an activity responsible for the error-prone repair of ultraviolet-induced lesions in deoxyribonucleic acid but is not involved in a cell's resistance to the lethal effects of ultraviolet light. RAD6B codes for an activity essential for error-free repair of potentially lethal mutagenic damage.
测定了酿酒酵母RAD6⁺基因的两个突变等位基因对赭石型翻译抑制因子SUQ5的反应。在[psi⁺]背景下,rad6-1等位基因的紫外线敏感性表型和紫外线诱导诱变表型的缺陷均被抑制。对于rad6-3等位基因,在[psi⁺]背景下只有紫外线敏感性表型可被抑制。检测的一株SUQ5 rad6-3 [psi⁺]菌株在紫外线诱导诱变方面表现出正常的rad6-3缺陷。我们提出RAD6⁺基因分为两个顺反子,即RAD6A和RAD6B。RAD6A编码一种负责DNA中紫外线诱导损伤的易错修复的活性,但不参与细胞对紫外线致死效应的抗性。RAD6B编码一种对潜在致死诱变损伤的无差错修复至关重要的活性。