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Biomedical subjects

K C Smith

Publications and source records attributed to K C Smith.

At least 217 records · Page 12Linked to original sources
PubMed1974

Separate branches of the uvr gene-dependent excision repair process in ultraviolet-irradiated Escherichia coli K-12 cells; their dependence upon growth medium and the polA, recA, recB, and exrA genes.

The extent of repair of single-strand breaks (incision breaks) induced in the deoxyribonucleic acid (DNA) of Escherichia coli K-12 cells by the uvr gene-dependent excision repair process after ultraviolet (UV) radiation was determined in the wild-type, polA1, recA56, recB21, and exrA strains. The wild-type strain repaired all incision breaks after incident doses of UV radiation (254 nm) of approximately 60 J m(-2) or less when incubated in growth medium, or approximately 15 J m(-2) or less when incubated in buffer. The polA1 strain repaired the incision breaks completely after incident doses of approximately 12 J m(-2) or less when incubated in growth medium, or after approximately 4 J m(-2) when incubated in buffer. The recA13, recB21, and exrA strains showed essentially complete repair after incident doses of 10 to 15 J m(-2) whether the cells were incubated in buffer or growth medium. These results suggest that the uvr gene-dependent excision repair process may be divided into two branches, one which is dependent on the presence of growth medium and also the rec(+)exr(+) genotype, and a second which can occur in buffer (growth medium-independent) and is largely dependent on DNA polymerase I. The presence of chloramphenicol in the growth medium resulted in an inhibition of the growth medium-dependent repair occurring in wild-type and polA1 cells and had little or no effect on the extent of repair observed in recA56, recB21, or exrA cells. The similarities between the growth medium-dependent and -independent branches of excision repair and two known processes for the repair of X-ray-induced single-strand breaks are discussed.

Buffers↗
PubMed1973

X-ray sensitivity and repair capacity of a polA1 exrA strain of Escherichia coli K-12.

A polA1 exrA strain of Escherichia coli K-12 was constructed. It was found to be more sensitive to aerobic or anoxic X irradiation than were mutants containing either polA1 or exrA alone. The ability of polA1 exrA and related strains to repair X-ray-induced single-strand breaks in deoxyribonucleic acid DNA was examined. The polA1 strain was deficient in type II (buffer) repair but not in type III (growth medium-dependent) repair. The exrA strain was not deficient in type II repair but was deficient in type III repair (similar to rec strains). The double mutant polA1 exrA was deficient in both type II and type III repair. Thus, the increased X-ray sensitivity of the polA1 exrA double mutant was correlated with its decreased ability to repair X-ray-induced single-strand breaks in DNA. We have tested the hypothesis that polA rec double mutants are not viable because they lack the types II and III systems for the repair of DNA single-strand breaks. Since the polA1 exrA strain is viable and is deficient in both of these repair processes, this hypothesis seems not to be correct.

Aerobiosis↗
PubMed1973

Evidence for the control by exrA and polA genes of two branches of the uvr gene-dependent excision repair pathway in Escherichia coli K-12.

A polA1 exrA strain of Escherichia coli K-12 was found to be more sensitive to ultraviolet radiation than the closely related polA1 or exrA strains, but not as sensitive as either the exrA uvrB or recA strains. The exrA and polA1 mutations both resulted in a deficiency in the repair of single-strand breaks arising in the deoxyribonucleic acid as a result of the excision repair process (incision breaks). These deficiencies were at least partially independent since the double mutant, polA1 exrA, was more deficient than a strain containing either the polA1 or exrA mutation alone. These results suggest that the polA1 and exrA mutations result in defects in two different branches of the uvr gene-dependent excision repair process. The repair of incision breaks was still observed in the polA1 exrA strain after low exposures of ultraviolet radiation, suggesting the existence of a third branch of the excision repair process which is dependent on neither the polA nor exrA genes. The polA1 and polA1 uvrA strains were not deficient in post-replicational repair. The exrA strain was partially deficient in post-replicational repair, but the polA1 exrA strain was no more deficient than the exrA strain in this repair process. Thus, the increased ultraviolet irradiation sensitivity of the polA1 exrA strain relative to the polA1 and exrA strains appears to be related to the effect of the polA1 and exrA mutations on different branches of the uvr gene-dependent excision repair process as well as to the effect of the exrA mutation on the post-replicational repair process.

Cell Survival↗
PubMed1972

Requirement for protein synthesis in rec-dependent repair of deoxyribonucleic acid in Escherichia coli after ultraviolet or X irradiation.

Deprivation of amino acids required for growth or treatment with chloramphenicol or puromycin after irradiation reduced the survival of Rec(+) cells of Escherichia coli K-12 which had been exposed to either ultraviolet (UV) or X radiation. In contrast, these treatments caused little or no reduction in the survival of irradiated recA or recB mutants. The effect of chloramphenicol on the survival of X-irradiated cells was correlated with an inhibition of repair of single-strand breaks in irradiated deoxyribonucleic acid (DNA), previously shown to be controlled by recA and recB. In UV-irradiated cells no effect of chloramphenicol was detected on the repair of single-strand discontinuities in DNA replicated from UV-damaged templates, a process controlled by recA but not by recB. From this we concluded that inhibiting protein synthesis in UV or X-irradiated cells may interfere with some biochemical step in repair dependent upon the recB gene. When irradiated Rec(+) cells were cultured for a sufficient period of time in minimal growth medium before chloramphenicol treatment their survival was no longer decreased by the drug. After X irradiation this occurred in less than one generation time of the unirradiated control cells. After UV irradiation it occurred more slowly and was only complete after several generation times of the unirradiated controls. These observations indicated that replication of the entire irradiated genome was probably not required for rec-dependent repair of X-irradiated cells, although it might be required for rec-dependent repair of UV-irradiated cells.

Amino Acids↗