Studies on the Inducible Inhibitor of Radiation-Induced DNA Degradation of Escherichia coli

Pollard, Ernest C.; Randall, Eleanor P.

doi:10.2307/3573682

Cited by 61 publications

(24 citation statements)

References 14 publications

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“…This would indicate either that the preinduced level of the protein is sufficient to control the exonuclease activity generated by a low UV dose or that the exonuclease only operates at higher UV doses. A similar enhancement of DNA degradation by chloramphenicol after UV irradiation is known in E. coli (18), and it has been suggested that normally the recA protein (24) or the ssb protein (12) 5. Appearance of label in medium containing chloramphenicol after irradiation of D. radiodurans strains.…”

mentioning

confidence: 55%

Roles of the uvsC, uvsD, uvsE, and mtcA genes in the two pyrimidine dimer excision repair pathways of Deinococcus radiodurans

Evans¹,

Moseley²

1983

J Bacteriol

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In Deinococcus radiodurans, the genes uvsC, uvsD, uvsE, and mtcA are all involved in the single-strand incision of UV-irradiated DNA, and mutations in at least two of them were required to produce an incisionless strain. One mutation must be in mtcA and one in uvsC, uvsD, or uvsE. Strains carrying single mutations in any one of the genes can incise DNA to the same extent as the wild-type strain. Neither the presence of EDTA nor the absence of protein synthesis affected the incision step. Strains deficient in DNA incision have greatly reduced DNA degradation after UV irradiation, and upon addition of chloramphenicol to the postirradiation medium, they do not undergo excessive DNA degradation as is seen in the wild-type strain and strains singly mutant in uvsC, uvsD, or uvsE. The strain singly mutant in mtcA also lacked chloramphenicol-enhanced DNA degradation and loss of viability but behaved similarly to the wild-type strain with respect to resumption of DNA synthesis and DNA degradation in the absence of chloramphenicol. It is proposed that two constitutive, cation-independent UV endonucleases are present in D. radiodurans: UV endonuclease a (the product of the mtcA gene), which incises in response to pyrimidine dimers, mitomycin C cross-links, bromomethylbenzanthracene adducts, and other alkylation damage, and UV endonuclease ,B (the product of the uvsC, uvsD, and uvsE genes), which incises only in response to pyrimidine dimers. Both endonucleases have associated exonuclease activity. The exonucleolytic activity associated with UV endonuclease a requires a UV-induced protein to terminate (or control) its activity, whereas the exonucleolytic activity associated with UV endonuclease v is slower acting and does not require the inducible terminator.

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mentioning

confidence: 55%

Roles of the uvsC, uvsD, uvsE, and mtcA genes in the two pyrimidine dimer excision repair pathways of Deinococcus radiodurans

Evans¹,

Moseley²

1983

J Bacteriol

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“…For cells undergoing inducing treatment, the required UV dose, varied to fit the strain, was given. Previous studies (Pollard and Randall, 1973) show that for UV induction of the induced inhibitor there is a maximum at about 15 J/m2 for wild-type strains and 1.5-2 J/m2 for uvr-strains. After the UV treatment, the cells were bubbled with air at 370C for 40 min to allow for synthesis of all induced proteins.…”

Section: Methodsmentioning

confidence: 92%

“…The work of Grady and Pollard (1968) confirmed these findings and suggested that radiation acts to cause the initiation of DNA degradation and to induce a factor controlling the amount of degradation as well. Pollard and Randall (1973), using preliminary UV treatment, together with a subsequent prevention of transcription with rifampin, demonstrated the time-course of its induction and some of the strains in which it was found. Marsden et al (1974) showed that the induction of the inhibitor of degradation could not be found in cells that were recAor lex-, suggesting that these genes were involved with the inhibition.…”

mentioning

confidence: 99%

“…More recently, it has become established that some cells respond to agents that damage their DNA, such as ultraviolet (UV), and subsequently express what is believed to be a coordinately regulated group of functions. Strains of E. coli that are recA+ and lex+ show several UV-inducible functions, including induction of prophage X, reactivation of irradiated phage (Weigle, 1953), induction of filament formation (Witkin, 1967), inhibition of postirradiation DNA degradation (Pollard and Randall, 1973), and an error-prone DNA repair activity related to mutation (Witkin and George, 1973). These are sometimes referred to as "s.o.s."…”

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confidence: 99%

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Relative rates of repair of single-strand breaks and postirradiation DNA degradation in normal and induced cells of Escherichia coli

Pollard¹,

Fugate²

1978

Biophysical Journal

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Labeled DNA from irradiated Excherichia coli cells has been studied on an alkaline sucrose gradient without acid precipitation of the DNA. This enables the observation of both DNA repair and DNA degradation. The use of a predose of ultraviolet light (UV) causes induction of an inhibitor of postirradiation DNA degradation in lex+ strains. The effect of this induction on both the repair of single-strand breaks and DNA degradation has been followed in strains WU3610 (uvr+) and WU3610-89 (uvr-). The repair process is more rapid than the degradation, and when degradation is inhibited more repair is apparent. Cells that are lex- (Bs-1 and AB2474) cannot be induced for inhibition of degradation. Nevertheless, by observation at short times repair can be seen clearly. This repaired DNA is degraded, suggesting that the signal for DNA degradation is not a single-strand break.

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“…In an attempt to explain this observation, we suggest that the recA product itself, which is known to be induced and accumulated in tifcells at 410C (12, 13) and to limit in vivo DNA breakdown (27), may contribute to the amount of extra repair observed. The same explanation can be applied to the fact that pre-irradiation with UV light causes a subsequent increase in survival after -y-ray irradiation (21); in this case, this "UV-stimulated" bacterial reactivation after yirradiation has been correlated (i) with an increased repair of single-strand breaks (29) and (ii) with a lower level of DNA degradation (22). This bacterial reactivation process has further been found (i) to be dependent upon de novo protein synthesis, (ii) not to be associated with mutagenesis, and (iii) to take place only in an excision-proficient uvrA' cell.…”

mentioning

confidence: 97%

tif-Stimulated deoxyribonucleic acid repair in Escherichia coli K-12

Castellazzi¹,

Jacques²,

George³

1980

J Bacteriol

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Bacterial survival is significantly increased after ultraviolet irradiation in tif sfi cells, provided that the thermosensitive tif mutation has been expressed at 410C before irradiation. This tif-mediated "reactivation of ultraviolet irradiated bacteria" needs de novo protein synthesis, as is the case for the tif-mediated reactivation of ultraviolet-irradiated phage A. However, in striking contrast to the phage reactivation process, this tif-mediated reactivation is no longer associated with mutagenesis. It also requires the presence of the uvrA' excision function. These results strongly suggest the existence in Escherichia coli K-12 of a repair pathway acting on bacterial deoxyribonucleic acid which is inducible, error free, and uvr dependent.

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Studies on the Inducible Inhibitor of Radiation-Induced DNA Degradation of Escherichia coli

Cited by 61 publications

References 14 publications

Roles of the uvsC, uvsD, uvsE, and mtcA genes in the two pyrimidine dimer excision repair pathways of Deinococcus radiodurans

Roles of the uvsC, uvsD, uvsE, and mtcA genes in the two pyrimidine dimer excision repair pathways of Deinococcus radiodurans

Relative rates of repair of single-strand breaks and postirradiation DNA degradation in normal and induced cells of Escherichia coli

tif-Stimulated deoxyribonucleic acid repair in Escherichia coli K-12

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