2,4-Dinitrophenol (DNP) (3× 10-3 M), when added to growth medium for 90 min of postirradiation incubation, markedly potentiated the x-ray induced killing of E. coli K-12 "wild-type," polAl and uvrB5 cells. The recA13, recB21, and exrA mutants, which are deficient in the slow, growth-medium dependent (Type III) repair of x-ray-induced DNA single-strand breaks, did not show radiation sensitization by DNP. In the polAl background, DNP treatment was as effective as an exrA mutation in sensitizing polAl cells to killing by x-rays. Alkaline sucrose gradient studies showed that DNP inhibited the Type III repair of single-strand breaks. This inhibition was largely irreversible.

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