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大肠杆菌中复制后修复的一条次要途径独立于recB、recC和recF基因。

A minor pathway of postreplication repair in Escherichia coli is independent of the recB, recC and recF genes.

作者信息

Sharma R C, Smith K C

出版信息

Mutat Res. 1985 Sep;146(2):169-76. doi: 10.1016/0167-8817(85)90007-0.

DOI:10.1016/0167-8817(85)90007-0
PMID:2993878
Abstract

After ultraviolet (UV) irradiation, an Escherichia coli K12 uvrB5 recB21 recF143 strain (SR1203) was able to perform a limited amount of postreplication repair when incubated in minimal growth medium (MM), but not if incubated in a rich growth medium. Similarly, this strain showed a higher survival after UV irradiation if plated on MM versus rich growth medium (i.e., it showed minimal medium recovery (MMR]. In fact, its survival after UV irradiation on rich growth medium was similar to that of a uvrB5 recA56 strain, which does not show MMR or postreplication repair. The results obtained with a uvrB5 recF332::Tn3 delta recBC strain and a uvrB5 recF332::Tn3 recB21 recC22 strain were similar to those obtained for strain SR1203, suggesting that the recB21 and recF143 alleles are not leaky in strain SR1203. The treatment of UV-irradiated uvrB5 recB21 recF143 and uvrB5 recF332::Tn3 delta recBC cells with rifampicin for 2 h had no effect on survival or the repair of DNA daughter-strand gaps. Therefore, a pathway of postreplication repair has been demonstrated that is constitutive in nature, is inhibited by postirradiation incubation in rich growth medium, and does not require the recB, recC and recF gene products, which control the major pathways of postreplication repair.

摘要

紫外线(UV)照射后,大肠杆菌K12 uvrB5 recB21 recF143菌株(SR1203)在基本生长培养基(MM)中培养时能够进行有限量的复制后修复,但在丰富生长培养基中培养时则不能。同样,该菌株在紫外线照射后接种于MM上的存活率高于丰富生长培养基(即,它表现出基本培养基恢复(MMR))。事实上,其在丰富生长培养基上紫外线照射后的存活率与uvrB5 recA56菌株相似,该菌株不表现出MMR或复制后修复。用uvrB5 recF332::Tn3 delta recBC菌株和uvrB5 recF332::Tn3 recB21 recC22菌株获得的结果与菌株SR1203的结果相似,表明recB21和recF143等位基因在菌株SR1203中不是渗漏的。用利福平处理紫外线照射后的uvrB5 recB21 recF143和uvrB5 recF332::Tn3 delta recBC细胞2小时,对存活率或DNA子链缺口的修复没有影响。因此,已经证明了一种复制后修复途径,其本质上是组成型的,受到照射后在丰富生长培养基中培养的抑制,并且不需要控制复制后修复主要途径的recB、recC和recF基因产物。

相似文献

1
A minor pathway of postreplication repair in Escherichia coli is independent of the recB, recC and recF genes.大肠杆菌中复制后修复的一条次要途径独立于recB、recC和recF基因。
Mutat Res. 1985 Sep;146(2):169-76. doi: 10.1016/0167-8817(85)90007-0.
2
Repair of DNA double-strand breaks in UV-irradiated Escherichia coli uvrB recF cells is inhibited by rich growth medium.富含营养的生长培养基会抑制紫外线照射的大肠杆菌uvrB recF细胞中DNA双链断裂的修复。
Mutat Res. 1986 Jul;166(1):23-8. doi: 10.1016/0167-8817(86)90037-4.
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Uvr-independent repair of 8-methoxypsoralen crosslinks in Escherichia coli: evidence for a recombinational process.大肠杆菌中8-甲氧基补骨脂素交联的不依赖紫外线的修复:重组过程的证据。
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Mechanism of sbcB-suppression of the recBC-deficiency in postreplication repair in UV-irradiated Escherichia coli K-12.紫外线照射的大肠杆菌K-12中sbcB抑制recBC缺陷在复制后修复中的机制。
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recA (Srf) suppression of recF deficiency in the postreplication repair of UV-irradiated Escherichia coli K-12.recA(Srf)对紫外线照射的大肠杆菌K-12复制后修复中recF缺陷的抑制作用。
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recA-dependent DNA repair in UV-irradiated Escherichia coli.紫外线照射的大肠杆菌中依赖RecA的DNA修复
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Mechanisms for recF-dependent and recB-dependent pathways of postreplication repair in UV-irradiated Escherichia coli uvrB.紫外线照射的大肠杆菌uvrB中复制后修复的recF依赖性和recB依赖性途径的机制。
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Different effects of recJ and recN mutations on the postreplication repair of UV-damaged DNA in Escherichia coli K-12.recJ和recN突变对大肠杆菌K-12中紫外线损伤DNA复制后修复的不同影响。
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Involvement of RecB-mediated (but not RecF-mediated) repair of DNA double-strand breaks in the gamma-radiation production of long deletions in Escherichia coli.RecB介导(而非RecF介导)的DNA双链断裂修复参与大肠杆菌中γ辐射诱导的长片段缺失的产生。
Mutat Res. 1992 Jan;265(1):83-101. doi: 10.1016/0027-5107(92)90041-y.

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Mechanism of sbcB-suppression of the recBC-deficiency in postreplication repair in UV-irradiated Escherichia coli K-12.紫外线照射的大肠杆菌K-12中sbcB抑制recBC缺陷在复制后修复中的机制。
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Role of DNA polymerase I in postreplication repair: a reexamination with Escherichia coli delta polA.
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J Bacteriol. 1987 Oct;169(10):4559-64. doi: 10.1128/jb.169.10.4559-4564.1987.
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Mol Gen Genet. 1988 Oct;214(2):198-203. doi: 10.1007/BF00337711.