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J Bacteriol. 1979 Apr;138(1):273-4. doi: 10.1128/jb.138.1.273-274.1979.
2
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The SOS Response Master Regulator LexA Regulates the Gene Transfer Agent of Rhodobacter capsulatus and Represses Transcription of the Signal Transduction Protein CckA.SOS 反应主调节因子 LexA 调控荚膜红细菌的基因转移因子并抑制信号转导蛋白 CckA 的转录。
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本文引用的文献

1
Ultraviolet light-induced mutation in UV-resistant, thermosensitive derivatives of lexA-strains of Escherichia coli K-12.紫外线诱导的大肠杆菌K-12 lexA菌株抗紫外线、温度敏感衍生物中的突变。
Mol Gen Genet. 1975;136(2):95-106. doi: 10.1007/BF00272033.
2
Suppression of lex mutations affecting deoxyribonucleic acid repair in Escherichia coli K-12 by closely linked thermosensitive mutations.通过紧密连锁的温度敏感突变抑制影响大肠杆菌K-12中脱氧核糖核酸修复的lex突变。
J Bacteriol. 1973 Nov;116(2):950-6. doi: 10.1128/jb.116.2.950-956.1973.
3
Dominant mutations (lex) in Escherichia coli K-12 which affect radiation sensitivity and frequency of ultraviolet lght-induced mutations.大肠杆菌K-12中影响辐射敏感性和紫外线诱导突变频率的显性突变（lex）
J Bacteriol. 1972 Nov;112(2):886-93. doi: 10.1128/jb.112.2.886-893.1972.
4
Production of cells without deoxyribonucleic acid during thymidine starvation of lexA- cultures of Escherichia coli K-12.在大肠杆菌K-12的lexA-培养物胸腺嘧啶核苷饥饿期间产生不含脱氧核糖核酸的细胞。
J Bacteriol. 1975 Dec;124(3):1113-21. doi: 10.1128/jb.124.3.1113-1121.1975.
5
Ultraviolet mutagenesis and inducible DNA repair in Escherichia coli.大肠杆菌中的紫外线诱变与诱导性DNA修复
Bacteriol Rev. 1976 Dec;40(4):869-907. doi: 10.1128/br.40.4.869-907.1976.
6
Analysis of cell division in single clones of the Escherichia coli K-12 lexA mutant.大肠杆菌K-12 lexA突变体单克隆中细胞分裂的分析。
J Bacteriol. 1978 Mar;133(3):1278-81. doi: 10.1128/jb.133.3.1278-1281.1978.

大肠杆菌K-12的lexA突变体培养物中细胞长度的分布。

Distribution of cell lengths in cultures of a lexA mutant of Escherichia coli K-12.

作者信息

Howe W E, Mount D W

出版信息

J Bacteriol. 1979 Apr;138(1):273-4. doi: 10.1128/jb.138.1.273-274.1979.

DOI:10.1128/jb.138.1.273-274.1979
PMID:374373
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC218272/
Abstract

Distributions of cell lengths in lexA+ and lexA mutant cultures during normal growth and under thymidine starvation conditions are presented. During normal growth lexA mutant cells were slightly shorter, on the average, than were lexA+ cells. lexA mutant cells were also shorter in comparison with lexA+ cells after a period of thymidine starvation. These results are consistent with the hypothesis that the lexA gene is involved in the coordination of cell division with DNA repair.

摘要

文中呈现了在正常生长以及胸腺嘧啶核苷饥饿条件下，lexA+和lexA突变体培养物中细胞长度的分布情况。在正常生长过程中，lexA突变体细胞平均而言比lexA+细胞略短。经过一段时间的胸腺嘧啶核苷饥饿处理后，与lexA+细胞相比，lexA突变体细胞也更短。这些结果与lexA基因参与细胞分裂与DNA修复的协调这一假设相一致。