However, it has been found that the occurrence of mutations could be placed under control in a repression protein Lex A that suppresses mutant polymerases II, IV and V. This opens a new way for fighting antibiotic resistance. It is being explored if the option of suppressing mutations via Lex A is viable. One primary concern would be if there are other ways of increasing mutations apart from Lex A.
One of such commonly cited mechanism is via methyl-directed mismatch repair (NMR) which was found to also be dependent on the cleavage of Lex A and derepression of mutant polymerases after exposure to Ciprofloxacin. This finding raises the possibility that being able to prevent the cleavage of Lex A may ultimately help to slow down antibiotic resistance. This could be work if different triggers and different mechanisms which lead to the increase of mutations, depend on the cleavage of Lex A as a crucial control for increasing mutations. For example, resistance to beta-lactams also which appear to require the cleavage of Lex A could be stopped.
Topic: Directed Evolution SOS
Primary source: Cirz R. T., Chin J. K., Andes D. R., Crecy-Lagard V., Craig W. A. & Romesberg F. E. (2005). Inhibition of mutation and combating the evolution of antibiotic resistance. PLOS Biology. 3 (6). e176 here
Secondary source: Cirz R. & Romesberg F. E. (2006). Induction and inhibition of ciprofloxacin resistance-conferring mutations in hypermutator bacteria. Antimicrobial Agents And Chemotherapy. 50 (1). 220-225 here
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