Repair of x-ray damage to bacterial DNA

Journal Article · Sun Jul 01 04:00:00 EDT 1973 · Curr. Top. Radiat. Res. Quart., v. 8, no. 4, pp. 351-399

OSTI ID:4405831

Town, C D; Smith, K C; Kaplan, H S

Of the lesions produced in DNA by ionizing radiation, the one most extensively studied to date, and most closely correlated with cell killing, is the breakage of one or both strands of the sugar-phosphate backbone. DNA strand breaks may occur in different locations, with corresponding differences in the size of the strand interruption and in the chemical nature of the residual end groups. These differences call different enzymes systems into play to restore the integrity of the polynucleotide chaln. Unrepaired single-strand breaks in DNA may be lethal for the cell; cell killing is significantly increased when repair is genetically or physiologically deficient or is inhibited by post- irradiation treatment with certain chemicals. Using selected mutants of Escherichia coli, it has been shown that essentially the same numbers of single- strand breaks are produced by x rays in the presence or absence of oxygen. After irradiation, these are rejoined to different extents by three operationally distinct repair processes, designated Types I, II and III. Type I repair, the fastest, goes to completion in less than one minute at 0 deg C. Since it preferentially rejoins breaks produced under anoxic conditions, its effect is to leave about one-third as many single-strand breaks remaining in cells irradiated under anoxic versus aerobic conditions. Preliminary evidence guggests that it may involve the action of DNA polynucleotide ligase. Of the breaks remaining unrepaired, whether produced anoxically or aerobically, about 90% are acted upon by the Type II system, which is also relatively fast (T/sub 1/2 = ~ 1-2 min at room temperature), does not require growth medium, and is largely deficiert in polA mutants. Type III repair requires 30-60 min of incubstion in growth medium at 37 deg C. It is absent in exr mutants and also in recA mutants which are deficient in genetic recombtnation. It is capable of repairing only a small fixed number of breaks (approximately 2 breaks per single-strand genome), whether produced anoxically or aerobically. Genetic and pharmacological evidence suggests that the recA gene is also required in an additonal repair process, which does not involve DNA single-strand breaks. Scveral recently developed experimental systems which may permit the further elucidation of these enzymatic repair processes under partially in vitro conditions are discussed. (auth)

• Research Organization: Stanford Univ., CA
• NSA Number: NSA-29-002845
• OSTI ID: 4405831
• Journal Information: Curr. Top. Radiat. Res. Quart., v. 8, no. 4, pp. 351-399, Journal Name: Curr. Top. Radiat. Res. Quart., v. 8, no. 4, pp. 351-399; ISSN CTRQA
• Country of Publication: Country unknown/Code not available
• Language: English

Related Subjects

BIOLOGICAL RADIATION EFFECTS
CELL KILLING
ESCHERICHIA COLI
MOLECULAR STRUCTURE
MUTANTS
N48310* --Life Sciences--Radiation Effects on Microorganisms- -Basic Studies
OXYGEN
PHOTON BEAMS
RADIOINDUCTION
RADIOSENSITIVITY EFFECTS
RESPONSE MODIFYING FACTORS
REVIEWS
X RADIATION