An assessment of the importance of error-prone repair and point mutations to forward mutation to L-azetidine-2-carboxylic acid resistance in Escherichia coli.
By comparison of E. coli WP2 with CM891 (uvrA- pKM101) we found that pKM101 plasmid and uvrA- mutation considerably enhanced both spontaneous and chemically-induced reversion at the trp locus. However, little or no increase was observed for forward mutation at the A2C locus. Furthermore, mutation frequency decline was considerably greater for trp reversion than for mutation to A2Cr. Thus neither error-prone repair nor point mutation seemed likely to be the major mechanism for forward mutation at the A2C locus. Results for spontaneous mutation of recA-, polA- and gyrA- strains showed that polA- and gyrA- gave good increases in forward mutation but not in reversion. It was inferred that deletion, transposition and/or larger chromosomal effects rather than point mutation were mainly responsible for most forward mutation.
Mitchell
I D
ID
Gilbert
P J
PJ
D001383:Azetidinecarboxylic Acid / Q000633:toxicity*; D001385:Azetines / Q000633:toxicity*; D001426:Bacterial Proteins / Q000235:genetics; D004260:DNA Repair; D004352:Drug Resistance, Microbial; D004926:Escherichia coli / Q000187:drug effects / Q000235:genetics*; D009154:Mutation; D010957:Plasmids
D001385:Azetines; D001426:Bacterial Proteins; D001383:Azetidinecarboxylic Acid