PROPHAGE INDUCTION AND CELL-DIVISION IN ESCHERICHIA-COLI .1. FURTHER CHARACTERIZATION OF THERMOSENSITIVE MUTATION TIF-1 WHOSE EXPRESSION MIMICS EFFECT OF UV IRRADIATION
PROPHAGE INDUCTION AND CELL-DIVISION IN ESCHERICHIA-COLI .1. FURTHER CHARACTERIZATION OF THERMOSENSITIVE MUTATION TIF-1 WHOSE EXPRESSION MIMICS EFFECT OF UV IRRADIATION
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DOI：
10.1007/bf00269133
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发表时间：
1972-01-01
期刊：
影响因子：
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通讯作者：
GEORGE, J
中科院分区：
文献类型：
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作者：
CASTELLAZZI, M;BUTTIN, G;GEORGE, J
一个明显的单一多效性突变tif-1引起λ的热诱导和热诱导，被定位在recA附近，并被证明是E的热敏表型的原因。coliC 600 T44（Goldthwait和Jacob，1964）。tif-1突变的表达模拟了紫外线照射在引起几种recA+依赖性事件中的作用：（1）原噬菌体诱导（2）细胞诱导（Goldthwait和Jacob，1964，Kirby，Jacob和Goldthwait，1967），（3）感染紫外线照射的λ噬菌体的存活，（4）紫外线照射的λ的诱变。tif-1突变的表达在两个方面不同于UV照射的作用：（1）如生物化学测量的，其对细菌DNA结构没有明显的作用（Kirbyet等人，1967; Ruffet等人，1971），或在生理学上通过DNA的接合转移能力或通过引起λ的间接诱导的能力来测量，λ的间接诱导通常发生在将UV照射的性因子引入溶原性F−受体之后（乔治and Devoret，1971）（2）它不增加F-lac+附加体与染色体之间或两个重组缺陷型λint reducer之间的A+依赖性重组。这些结果表明，thetif+基因产物参与的反应共同的紫外线诱导的途径和紫外线诱导的DNA损伤的修复途径。
An apparently single pleiotropic mutationtif-1causingthermalinduction of λ and thermalfilamentation is mapped close torecAand is shown to be responsible for the thermosensitive phenotype ofE. coliC 600 T44 (Goldthwait and Jacob, 1964). Expression of thetif-1mutation mimics the effect of UV irradiation in causing severalrecA+-dependent events: (1) prophage induction (2) cell filamentation (both previously observed by Goldthwait and Jacob, 1964, and by Kirby, Jacob and Goldthwait, 1967) and, (3) survival of infecting UV-irradiated bacteriophage λ, and (4) mutagenesis of UV-irradiated λ. Expression of thetif-1mutation differs from the effect of UV irradiation in two respects: (1) It has no apparent effect on bacterial DNA structure as measured biochemically (Kirbyet al., 1967; Ruffet al., 1971) or as measured physiologically here by the capacity for conjugal transfer of DNA or by the capacity for causing indirect induction of λ which normally occurs after the introduction of a UV-irradiated sexual factor into a lysogenic F−recipient (George and Devoret, 1971) (2) It does not increaserecA+-dependent recombination between an F-lac+episome and the chromosome or between two recombination deficient λint redphages. These results suggest that thetif+gene product participates in a reaction common to the pathway of UV induction and to the pathway of repair of UV-induced lesions in DNA.