Arthur H M, Lloyd R G
Mol Gen Genet. 1980;180(1):185-91. doi: 10.1007/BF00267368.
A mutant strain of E. coli which was isolated initially because of its strong hyper-recombination phenotype was shown to carry a lesion in uvrD. The presence of this mutation, designated uvrD210, increased the frequency of recombination between chromosomal duplications in F-prime repliconant cells and reduced linkage between closely linked markers in crosses with Hfr donors. A comparable hyper-rec phenotype was demonstrated in strains carrying other alleles of uvrD previously referred to as mutU4, uvr502 and recL152. The recombination activity of a uvrD210 strain was abolished by mutation of recA but the mutator activity associated with this allele proved to be independent of recA. It is suggested that uvrD mutations reduce the fidelity of DNA replication and that the accumulation of lesions in the newly synthesized strand provides additional sites for initiating recombination.
一种最初因其强烈的超重组表型而分离出的大肠杆菌突变菌株被证明在uvrD基因上存在损伤。这种名为uvrD210的突变的存在增加了F-prime复制子细胞中染色体重复序列之间的重组频率,并降低了与Hfr供体杂交时紧密连锁标记之间的连锁性。在携带uvrD其他等位基因(先前称为mutU4、uvr502和recL152)的菌株中也表现出类似的超重组表型。uvrD210菌株的重组活性因recA基因突变而被消除,但与该等位基因相关的诱变活性被证明独立于recA。有人提出,uvrD突变会降低DNA复制的保真度,并且新合成链中损伤的积累为启动重组提供了额外的位点。