scholarly journals Transcription increases methylmethane sulfonate-induced mutations in alkB strains of Escherichia coli

DNA Repair ◽  
2008 ◽  
Vol 7 (8) ◽  
pp. 1289-1297 ◽  
Author(s):  
Douglas Fix ◽  
Chandrika Canugovi ◽  
Ashok S. Bhagwat
2002 ◽  
Vol 184 (20) ◽  
pp. 5599-5608 ◽  
Author(s):  
Cesar Rodriguez ◽  
Joshua Tompkin ◽  
Jill Hazel ◽  
Patricia L. Foster

ABSTRACT Adaptive mutation to Lac+ in Escherichia coli strain FC40 depends on recombination functions and is enhanced by the expression of conjugal functions. To test the hypothesis that the conjugal function that is important for adaptive mutation is the production of a single-strand nick at the conjugal origin, we supplied an exogenous nicking enzyme, the gene II protein (gIIp) of bacteriophage f1, and placed its target sequence near the lac allele. When both gIIp and its target site were present, adaptive mutation was stimulated three- to fourfold. Like normal adaptive mutations, gIIp-induced mutations were recA+ and ruvC+ dependent and were mainly single-base deletions in runs of iterated bases. In addition, gIIp with its target site could substitute for conjugal functions in adaptive mutation. These results support the hypothesis that nicking at the conjugal origin initiates the recombination that produces adaptive mutations in this strain of E. coli, and they suggest that nicking may be the only conjugal function required for adaptive mutation.


1969 ◽  
Vol 46 (1) ◽  
pp. 17-23 ◽  
Author(s):  
Suzanne Sesnowitz-Horn ◽  
Edward A. Adelberg

1976 ◽  
Vol 147 (2) ◽  
pp. 203-208 ◽  
Author(s):  
Kazunori Shimada ◽  
Yasuyuki Fukumaki ◽  
Yasuyuki Takagi

Genetics ◽  
1984 ◽  
Vol 106 (3) ◽  
pp. 347-364
Author(s):  
Bernard A Kunz ◽  
Barry W Glickman

ABSTRACT We have employed conjugal transfer of an F′ lac episome to examine targeted and untargeted mutagenesis in the lacI gene of Escherichia coli and to determine the relative importance of pyrimidine dimers as premutational UV lesions compared to (6-4) photoproducts that also may have a mutational role. This conjugal system allowed us to assess the premutagenic role of UV lesions independently from any role as inducers of SOS functions. F′ DNA was transferred to an SOS-induced recipient strain from: unirradiated donor cells, UV-treated donor cells or donor cells that were irradiated and then exposed to photoreactivating light. The results indicate that SOS-related, untargeted events may account for as much as one-third of the nonsense mutations (i.e., base substitutions) recovered after undamaged F′ DNA is transferred to UV-irradiated recipients. When the donor strain also is irradiated, in excess of 90% of the mutations detected following conjugation appear to be targeted. Photoreactivation of the UV-treated donor cells, prior to F′ transfer to the SOS-induced recipient strain, demonstrated that in this experimental system virtually all recovered UV-induced mutations are targeted by photoreactivable lesions. We presume that these lesions are pyrimidine dimers because (6-4) photoproducts are not photoreactivable.


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