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在已知修复功能缺陷的大肠杆菌菌株中,R因子介导的对紫外线的抗性。

R factor-mediated resistance to ultraviolet light in strains of Escherichia coli deficient in known repair functions.

作者信息

Tweats D J, Thompson M J, Pinney R J, Smith J T

出版信息

J Gen Microbiol. 1976 Mar;93(1):103-10. doi: 10.1099/00221287-93-1-103.

Abstract

The expression of resistance to u.v. irradiation mediated by R factor R46 has been studied in strains deficient in excision repair and recombination repair. The R factor protected wild-type bacteria and also wild-type cells in which repair had been inhibited by the substitution of bromouracil for chromosomal thymine. It increased the survival of strains defective in the endonucleolytic (uvr), repolymerizing (pol) and joining (lig) stages of the excision repair process. Recombination deficient bacteria mutant at the recB or recC loci were protected by R46, but the R factor had little effect on the survival of a recA strain or a recA recB double mutant. R46 increased the survival of cells that had been treated with chloramphenicol before u.v. irradiation, but did not protect cultures treated with chloramphenciol after irradiation. It is concluded that R46 confers resistance to the lethal effects of u.v. irradiation by a mechanism that is independent of excision repair. Resistance appears to be mediated by an inducible gene product, which is possibly a nuclease and dependent on a functional host recA gene for expression.

摘要

在切除修复和重组修复缺陷的菌株中,对由R因子R46介导的紫外线照射抗性的表达进行了研究。R因子保护野生型细菌以及通过用溴尿嘧啶替代染色体胸腺嘧啶来抑制修复的野生型细胞。它提高了切除修复过程中核酸内切(uvr)、重新聚合(pol)和连接(lig)阶段存在缺陷的菌株的存活率。在recB或recC位点发生突变的重组缺陷细菌受到R46的保护,但R因子对recA菌株或recA recB双突变体的存活率几乎没有影响。R46提高了在紫外线照射前用氯霉素处理过的细胞的存活率,但不能保护照射后用氯霉素处理的培养物。得出的结论是,R46通过一种独立于切除修复的机制赋予对紫外线照射致死效应的抗性。抗性似乎由一种可诱导的基因产物介导,该产物可能是一种核酸酶,并且其表达依赖于功能性的宿主recA基因。

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