大肠杆菌WP2 uvrA的uvrD recB衍生物对紫外线的不可突变性是由于RecA蛋白激活受到抑制。

Non-mutability by ultraviolet light in uvrD recB derivatives of Escherichia coli WP2 uvrA is due to inhibition of RecA protein activation.

作者信息

Woodgate R, Bridges B A, Kelly C

机构信息

MRC Cell Mutation Unit, University of Sussex, Falmer, Brighton, Great Britain.

出版信息

Mutat Res. 1989 Jul;226(3):141-4. doi: 10.1016/0165-7992(89)90010-9.

DOI:10.1016/0165-7992(89)90010-9

PMID:2664496

Abstract

The deficiency in UV mutagenesis in uvrD3 recB21 strains of E. coli is almost completely overcome by constitutive activation of RecA protein and expression of the SOS system (by recA730 or 43 degrees C treated recA441 lexA71). When SOS was expressed but RecA protein not self-activated (recA441 lexA71 at 30 degrees C), uvrD3 recB21 still reduced UV mutagenesis at low doses. The uvrD3 recB21 combination is therefore inhibiting activation of RecA protein. It is suggested that the DNA unwinding activity of the products of the uvrD and recB genes may be involved in generating single-stranded DNA needed to activate RecA protein both for the cleavage of LexA repressor and for a further role in UV mutagenesis.

摘要

大肠杆菌uvrD3 recB21菌株中紫外线诱变缺陷几乎可通过RecA蛋白的组成型激活和SOS系统的表达（通过recA730或43℃处理的recA441 lexA71）而完全克服。当SOS表达但RecA蛋白未自我激活时（30℃下的recA441 lexA71），uvrD3 recB21在低剂量时仍会降低紫外线诱变。因此，uvrD3 recB21组合抑制了RecA蛋白的激活。有人提出，uvrD和recB基因产物的DNA解旋活性可能参与产生激活RecA蛋白所需的单链DNA，这对于LexA阻遏物的切割以及在紫外线诱变中的进一步作用均有必要。