DNA-replication recovery inhibition and subsequent reinitiation in UV-radiation-damaged E. coli: a strategy for survival.

Using the incorporation of [14C]thymine to measure DNA accumulation, it was shown that exposure of the B/r strain of Escherichia coli to 10 J/m2 of ultraviolet radiation (UV) inhibits replication for about 20 min, but then resumption of replication occurs. Pulse-labelling with [3H]thymidine after exposure of the WT strain to this fluence confirmed the transient inhibition and recovery of DNA replication. After recovery, the rate of accumulation of DNA in the culture increases, to exceed that of the exponentially growing culture, so that eventually the amount of DNA almost equals that of the unirradiated culture.

Evidence that ultraviolet light-induced DNA replication death of recA bacteria is prevented by protein synthesis in repair-proficient bacteria.

The ultraviolet light (UV) survival curve of Escherichia coli WP10 recA trp is almost biphasic, with a greatly reduced shoulder but demonstrating a transition to a decreased slope with increasing fluences, indicating the presence in the culture of a low frequency of resistant cells. Treatment of the culture with chloramphenicol before UV exposure brought almost all of the cells to a high degree of UV resistance, by bringing them to the end of their DNA replication cycle. The survival curves of the repair-proficient E.

Modification of survival after ultraviolet light exposure in a wild-type and a polA strain of Escherichia coli B/r by preirradiation treatment with chloramphenicol or rifampin.

The shoulder of the UV fluence-survival curve of exponentially growing Escherichia coli B/r WP2 trpE65 was expanded by chloramphenicol pretreatment and an exponential segment with intermediate slope appeared between the shoulder and the final exponential segment. These changes were dependent on DNA replication. The transitions with UV exposure to increased slopes were ascribed to UV inactivation of qualitatively different repair systems, each dependent upon the accumulation in each bacterium of multiple DNA-containing redundant repair components, which must be inactivated before the respective transitions to decreased resistance occur.

Chloramphenicol-promoted increase in resistance to UV damage in Escherichia coli B/r WP2 trpE65: development of the capacity for successful repair of otherwise mutagenic or lethal lesions in DNA.

The ultraviolet radiation survival curve of exponentially growing cultures of Escherichia coli B/r WP2 trpE65 was modified by a short period (20 min) of chloramphenicol treatment before UV exposure, which produced an extended exponential section of intermediate slope between the shoulder and the final exponential slope. More prolonged incubation with chloramphenicol (up to 90 min) resulted in little further extension of the intermediate exponential slope, but caused a progressive expansion of the shoulder region. With each period of chloramphenicol pretreatment, a major surge of mutation to tryptophan independence always occurred after that UV fluence promoting the transition from the shoulder to the intermediate exponential slope of the survival curve, and another major surge occurred after that fluence promoting the transition from the intermediate exponential slope to the final exponential slope.

Modification of UV-induced mutation frequency and cell survival of Escherichia coli B/r WP2 trpE65 by treatment before irradiation.

The UV radiation survival curve of exponentially growing cultures of Escherichia coli B/r WP2 trpE65 was modified by pretreatment for short incubation periods (up to 20 min) with chloramphenicol such that an extended exponential section of intermediate slope appeared between the shoulder and the final exponential slope. Surges of mutation to tryptophan independence occurred with each increase in slope of the survival curve. These surges were separated by extended sections of little mutation.