Li B H, Bockrath R
Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis 46202-5120, USA.
Mol Gen Genet. 1995 Dec 20;249(6):585-90. doi: 10.1007/BF00418027.
Mutation frequency decline (MFD) in Escherichia coli was examined for effects associated with genetic defects in mismatch repair. The kinetics of MFD are slower when the B/r strain WU3610 carries the mutation mutS201::Tn5 or mutL::Tn10, both of which affect mismatch repair. Similar slow kinetics are produced by mutH34 but not by mutH471::Tn5; the latter has no apparent effect. Strain WU3610-45 (mfd-1) produces the slower kinetics if transcription is inhibited during the post-UV incubation, although it produces no decline in normal circumstances. The slower kinetics are therefore attributed to bulk excision repair that remains when rapid transcription-coupled repair (TCR) is eliminated by certain defects in mismatch repair. A model is proposed wherein mismatch repair defects are thought to slow the activity of TCR but, unlike an mfd defect, not to impede dissociation of stalled transcription complexes at lesions in the transcribed DNA strand.
对大肠杆菌中的突变频率下降(MFD)进行了检查,以探究与错配修复基因缺陷相关的影响。当B/r菌株WU3610携带突变mutS201::Tn5或mutL::Tn10时,MFD的动力学较慢,这两种突变均影响错配修复。mutH34也会产生类似的缓慢动力学,但mutH471::Tn5则不会;后者没有明显影响。如果在紫外线照射后的孵育过程中抑制转录,菌株WU3610 - 45(mfd - 1)会产生较慢的动力学,尽管在正常情况下它不会出现下降。因此,较慢的动力学归因于当错配修复中的某些缺陷消除了快速转录偶联修复(TCR)时仍然存在的大量切除修复。提出了一个模型,其中错配修复缺陷被认为会减缓TCR的活性,但与mfd缺陷不同的是,不会阻碍转录DNA链上损伤处停滞的转录复合物的解离。