Anderson J A, Barbour S D
J Bacteriol. 1973 Jan;113(1):114-21. doi: 10.1128/jb.113.1.114-121.1973.
Thymine starvation of Escherichia coli K-12 results in greatly increased sensitivity to ultraviolet light (UV). Our studies, using isogenic strains carrying rec and uvr mutations, have shown the following. (i) Common to all strains tested is a change from multihit to single-hit kinetics of survival to UV after 60 min of thymine starvation. However, the limiting slope of UV survival curves decreases in the rec(+)uvr(+) strain and changes very little in several rec mutant strains and one uvrB mutant strain. Thus, when either the rec or uvr system is functioning alone, the limiting slopes of the UV survival curves are relatively unaffected by thymine starvation. (ii) Thymine starvation does not significantly inhibit repair processes carried out by either repair system alone; i.e., host cell reactivation of irradiated phage (carried out by the uvr system), excision of thymine dimers (uvr), or X-ray repair (rec). (iii) In a rec(+)uvr(+) strain, repair appears to be a synergistic rather than additive function of the two systems. However, after thymine starvation, repair capacity is reduced to about the sum of the repair capacities of the independent systems. (iv) The kinetics of thymineless death are not changed by rec and uvr mutations. This indicates that the lesions responsible for thymineless death are not repaired by rec or uvr systems. (v) Withholding thymine from thy rec(+)uvr(+) bacteria not undergoing thymineless death has no effect on UV sensitivity. Under these conditions one sees higher than normal UV resistance in the presence or absence of thymine. This is due to increased repair carried out by the uvr system. To explain these results we postulate that thymine starvation does not inhibit either the rec or uvr repair pathway directly. Rather it appears that thymine starvation results in increased UV sensitivity in part by inhibiting a function which normally carries out efficient coordination of rec and uvr pathways.
大肠杆菌K - 12的胸腺嘧啶饥饿会导致其对紫外线（UV）的敏感性大幅增加。我们使用携带rec和uvr突变的同基因菌株进行的研究表明了以下几点。（i）所有测试菌株的共同特征是，在胸腺嘧啶饥饿60分钟后，其对紫外线的存活动力学从多击转变为单击。然而，rec(+)uvr(+)菌株中紫外线存活曲线的极限斜率降低，而在几个rec突变菌株和一个uvrB突变菌株中变化很小。因此，当rec或uvr系统单独起作用时，紫外线存活曲线的极限斜率相对不受胸腺嘧啶饥饿的影响。（ii）胸腺嘧啶饥饿不会显著抑制单独由任何一个修复系统进行的修复过程；即，受辐照噬菌体的宿主细胞再激活（由uvr系统进行）、胸腺嘧啶二聚体的切除（uvr）或X射线修复（rec）。（iii）在rec(+)uvr(+)菌株中，修复似乎是这两个系统的协同功能而非相加功能。然而，胸腺嘧啶饥饿后，修复能力降低到独立系统修复能力之和左右。（iv）rec和uvr突变不会改变无胸腺嘧啶死亡的动力学。这表明导致无胸腺嘧啶死亡的损伤不能被rec或uvr系统修复。（v）对于未经历无胸腺嘧啶死亡的thy rec(+)uvr(+)细菌，停止供应胸腺嘧啶对紫外线敏感性没有影响。在这些条件下，无论有无胸腺嘧啶，都会观察到高于正常的紫外线抗性。这是由于uvr系统进行的修复增加。为了解释这些结果，我们假设胸腺嘧啶饥饿不会直接抑制rec或uvr修复途径。相反，胸腺嘧啶饥饿似乎部分通过抑制一种通常对rec和uvr途径进行有效协调的功能而导致紫外线敏感性增加。
