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大肠杆菌中的诱变DNA修复。十二。通过延迟光逆转揭示的切除能力正常的umuC和lexA(ind-)细菌中的紫外线诱变。

Mutagenic DNA repair in Escherichia coli. XII. Ultraviolet mutagenesis in excision-proficient umuC and lexA (ind-) bacteria as revealed by delayed photoreversal.

作者信息

Bridges B A, Sharif F

机构信息

MRC Cell Mutation Unit, University of Sussex, Brighton, UK.

出版信息

Mutagenesis. 1986 Mar;1(2):111-7. doi: 10.1093/mutage/1.2.111.

Abstract

Streptomycin-resistant mutations are induced in excision-proficient umuC122::Tn5 bacteria given delayed photoreversal after u.v. light. The mutations occur after much earlier photoreversal than is found with the similar induction of tryptophan-independent mutations in excision-deficient umuC bacteria and the process is not markedly influenced by the presence of Casamino acids. The yield of mutants is between 25 and 40% of that found immediately after u.v. irradiation of isogenic umu+ bacteria. Mutagenesis is not inhibited by the presence of chloramphenicol after u.v. and before photoreversal when the bacteria have also been pretreated with chloramphenicol. Loss of photoreversibility of streptomycin-resistant mutations in umu+ excision-proficient bacteria also occurs during a similar period after u.v. and is similarly unaffected by Casamino acids and chloramphenicol. The results are interpreted on a 2-step model of error-prone repair in which a misincorporation step is followed by a lesion bypass step which requires induced levels of umuC gene product, the latter step being unnecessary when the pyrimidine dimer is removed by photoreversal after the misincorporation has taken place. Differences from the same phenomenon in excision-deficient bacteria are accounted for by the fact that in excision-proficient bacteria the mutation process is initiated by excision repair rather than during normal chromosomal replication. It is suggested that loss of photoreversibility in excision-proficient umu+ bacteria may reflect the misincorporation step only, thus explaining the apparent non-inducible nature of loss of photoreversibility previously reported. The bypass step alone requires induced levels of umuD,C gene products as is evidenced by the u.v.-induction of mutations in lexA102(ind-) bacteria after delayed photoreversal.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

在紫外线照射后给予延迟光复活的情况下,在切除功能正常的umuC122::Tn5细菌中诱导出链霉素抗性突变。这些突变发生在比切除缺陷的umuC细菌中类似地诱导色氨酸非依赖型突变更早的光复活之后,并且该过程不受酪蛋白氨基酸存在的显著影响。突变体的产量是同基因umu⁺细菌紫外线照射后立即发现产量的25%至40%。当细菌也用氯霉素预处理后,紫外线照射后且在光复活之前存在氯霉素时,诱变作用不会受到抑制。在紫外线照射后的相似时间段内,umu⁺切除功能正常的细菌中链霉素抗性突变的光复活能力丧失也会发生,并且同样不受酪蛋白氨基酸和氯霉素的影响。结果基于易错修复的两步模型进行解释,其中错配掺入步骤之后是损伤绕过步骤,这需要诱导水平的umuC基因产物,当嘧啶二聚体在错配掺入发生后通过光复活被去除时,后一步骤是不必要的。切除缺陷细菌中同一现象的差异是由于在切除功能正常的细菌中,突变过程是由切除修复启动的,而不是在正常染色体复制期间。有人提出,切除功能正常的umu⁺细菌中光复活能力的丧失可能仅反映错配掺入步骤,从而解释了先前报道的光复活能力丧失明显不可诱导的性质。单独损伤绕过步骤需要诱导水平的umuD、C基因产物,这在延迟光复活后lexA102(ind-)细菌中紫外线诱导的突变中得到证明。(摘要截短至250字)

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