RESPIRATION RESPONSES OF A polA1 AND A tif‐1 MUTANT OF ESCHERICHIA COLI TO FAR‐ULTRAVIOLET IRRADIATION*

— Cessation of respiration in Escherichia coli 60min after far-ultraviolet (254 nm) irradiation is dependent upon the recA and lexA gene products and is regulated by cyclic 3′,5′-adenosine monophosphate (cAMP) and its receptor protein. Respiration responses to UV irradiation were studied in two E. coli B/r mutants, polA1 and tif-1, both of which express other rec/lex functions (such as mutagenesis) after UV irradiation. The cells were grown on glycerol minimal medium supplemented with required amino acids. After receiving a relatively high UV fluence, the polA1 mutant, deficient in DNA polymer-ase I, showed a respiration shutoff response like the wild type cells. 5-Fluorouracil and rifampin, an inhibitor of initiation of RNA synthesis, did not prevent respiration shutoff in the mutant cells as they did in the wild type cells. Thus, RNA synthesis is not necessary for cessation of respiration in polA1 cells and the process is not an induced one. At lower fluences which did not shut off respiration of polA1 cells, cAMP did not cause a more complete shutoff as it did for the wild type cells. The tif-1 mutant has a modified recA protein, and when unirradiated cells are incubated at 42°C they form filaments, mutate, and show other rec/lex responses. This mutant did not shut off its respiration at either 30 or 42°C, and the response was not modified by cAMP. An E. coli K12 strain, W3110, was also tested for its respiration response to UV. At 52J/m2 respiration did not shut off and cAMP had no effect.