https://mmbr.asm.org/content/mmbr/36/4/525.full.pdf

Pedigrees of some mutant strains of Escherichia coli K-12.

https://mmbr.asm.org/content/mmbr/48/1/60.full.pdf

Mutagenesis and inducible responses to deoxyribonucleic acid damage in Escherichia coli.

INTRODUCTION .............................................................. 869 Enzymatic Repair of UV Damage in E. coli ......... .......................... 869 Error-Proof and Error-Prone Pathways of DNA Repair ....... ................. 871 The \"SOS\" Hypothesis: the Regulatory Role of DNA Damage ...... ............ 874 EVIDENCE FOR THE INDUCIBILITY OF ERROR-PRONE REPAIR (\"SOS REPAIR\") ACTIVITY ..................................................... 875 SOS Repair of Bacteriophage DNA ............ ............................... 875 SOS Repair of Bacterial DNA ................ ................................ 876 Evidence from studies of repair-deficient mutants ....... .................... 876 Evidence from studies of postreplication repair ........ ...................... 879 MANIFESTATIONS OF SOS REPAIR AND THEIR SIGNIFICANCE ..... ...... 879 Mutation Frequency Response to Increasing Fluence of UV Radiation ..... ..... 879 The UV Lesion Responsible for Induction of SOS Functions.................... 880 Kinetics of Induction and Decay of SOS Repair Activity ....... ................ 882 Time of Action of SOS Repair in UV Mutagenesis ...... ........................ 882 Cryptic Premutational Lesions Susceptible to SOS Repair ...................... 884 Mutator Effect of SOS Repair on Undamaged DNA ....... ..................... 885 PLASMIDS AND SOS REPAIR ................................................ 886 MECHANISM OF SOS REPAIR ............................................... 886 Mechanism of SOS Repair in Bacteriophage ......... .......................... 886 Mechanism of SOS Repair in Bacteria ........... ............................. 887 IMPLICATIONS OF SOS REPAIR FOR CARCINOGENESIS ................... 888 REGULATION OF SOS REPAIR AND OTHER UV-INDUCIBLE FUNCTIONS . 889 PROTEASES AND THE EXPRESSION OF SOS FUNCTIONS .................. 894 CONCLUSIONS ............................................................... 895 APPENDIX................................................................... 896 LITERATURE CITED ......................................................... 898

Ultraviolet mutagenesis and inducible DNA repair in Escherichia coli.

Biochemistry of homologous recombination in Escherichia coli.

[This corrects the article on p. 116 in vol. 40.].

https://mmbr.asm.org/content/mmbr/40/1/116.full.pdf

Recalibrated linkage map of Escherichia coli K-12.

BACTERIA are readily killed by exposure to ultraviolet light (UV) , presumably as the result of the formation of UV photoproducts in the bacterial DNA. It is also known that pyrimidine dimers are among the photoproducts formed with a high yield, and that bacteria normally contain an efficient mechanism for the repair of DNA containing these products. Pyrimidine dimers are excised from DNA during incubation and can be recovered, still contained within a short oligonucleotide. This excision appears to involve the interruption of single DNA strands, and to be followed by local DNA breakdown and repair synthesis (SETLOW and CARRIER 1964; BOYCE and HOWARD-FLANDERS 1964; PETTIJOHN and HANAWALT 1964). These observations are of interest not only because they reveal the mechanism of an effective and possibly widespread process for the repair of injured DNA, but also because they suggest that local repair can occur in one strand of a double helix. This mechanism for DNA repair may be related to the mechanism of genetic exchange. An insight into the mechanisms of genetic recombination was gained through the discovery that h bacteriophage recombinants can be formed by joining fragments of preexisting phage DNA molecules (MESELSON and WEIGLE 1961). As continuity in the base sequence of the phage genome must be preserved, base pairing between overlapping single strands from each parentel molecule is presumably required as a prelude to the formation of a recombinant ( LEVINTHAL 1959). It has been suggested that the process of recombination may be completed by local DNA repair synthesis on either side of the overlap (MESELSON 1964) and that certain of the enzymes involved may serve in both genetic recombination and in repair after irradiation ( HOWARD-FLANDERS and BOYCE 1964). Further evidence in support of these concepts has been obtained through the isolation of mutants of E. coZi K-12 that have lost the ability to form recombinants when mated with suitable donor strains. As these mutants are able to accept genetic material normafly, it appears that they may be defective in the process of integrating the donor DNA into the recipient chromosome (phenotype symbol Kec-) . Because of the suggested relationship between repair and recombination, the strains were tested for ability to survive exposure to UV, and were found to be highly radiosensitive (CLARK and MARGULIES 1965). After exposure to UV, these mutants degrade their DNA excessively and fail to incorporate labeled thymidine ( CLARK, CHAMBERLIN, BOYCE, and HOWARD-FLANDERS 1966).

/pdf/mutants-of-escherichia-coli-k-12-defective-in-dna-repair-and-4cttq7yjlx.pdf

Mutants of escherichia coli k-12 defective in dna repair and in genetic recombination

LTRAVIOLET irradiation produces dimers of thymine, thymine-cytosine and cytosine in deoxyribonucleic acid (DNA) (BEUKERS, IJLSTRA and BERENDS 1960; WACKER, DELLWEG and WEINBLUM 1960; SETLOW, CARRIER and BOLLUM 1965). UV light inactivates transforming DNA and induces thymine dimers in a parallel manner, as if the dimers block transforming activity (SETLOW and SETLOW 1962). Thymine dimers and thymine-cytosine dimers are removed and probably monomerized by photoreactivation enzyme ( WULF and RUPERT 1962; SETLOW, CARRIER and BOLLUM 1965). They are excised from DNA during incubation in the dark in wild-type strains of E. coli. However, this excision does not occur in the radiosensitive mutants Bs.l and K-12 uvrA (SETLOW and CARRIER 1964; BOYCE and HOWARD-FLANDERS 1964a). T1 or A bacteriophage irradiated with ultraviolet light (UV) form more plaques when plated on wild-type cells than when plated on these radiosensitive mutants (ELLISON. FEINER and HILL 1960; HOWARD-FLANDERS, BOYCE, SIMSON and THERIOT 1962; RORSCH, EDELMAN and COHEN 1963; HARM 1963). These results may be explained if the irradiated phage DNA is reactivated (host cell reactivation) in wild-type hosts, but not in these UV-sensitive mutants. The reactivation of UV-irradiated T1 bacteriophage is controlled by three genetic loci, designated uLv-A, uvrB and uurC. the approximate map positions of which have been reported (HOWARD-FLANDERS 1964; VAN DE PUTTE, VAN SLUIS, VAN DILLEWIJN and RORSCH 1965). In the present paper, we report the genetic analysis of 23 such mutants, more accurate mapping by cotransduction of the uurA, uurB and the uurC loci with other markers, some properties of the double mutants that carry two uur mutations, and evidence that all three loci control the excision from DNA of UV-induced thymine dimers and thymine-cytosine dimers.

/pdf/three-loci-in-escherichia-coli-k-12-that-control-the-44zglzqhy8.pdf

Three loci in Escherichia coli K-12 that control the excision of pyrimidine dimers and certain other mutagen products from DNA.

Long form radiosensitive mutants were selected from among the progeny of survivors of an ultraviolet irradiated parental strain of E. coli K-12 by their mucoid appearance on supplemented minimal agar. The parental strain was F/sup -/ and carried various auxotrophic markers. Crosses with Hfr strains revealed that all the long-form cells carried a mutation at a locus designated lon, which is situated between lac and gal, close to T6. The parental lon/sup +/ strain resembles B/r in survival following x or uv irradiation, while lon mutants are relatively sensitive and are similar to strain B. The greater radiosensitivity of the lon mutants is not due to the loss of the capacity to reactivate uv- photoproducts in DNA because equal numbers of plaques are found when uv irradiated Tl phage is plated on lon and lon/sup +/ strains. (auth)

https://www.genetics.org/content/genetics/49/2/237.full.pdf

A locus that controls filament formation and sensitivity to radiation in escherichia coli k-12.

Strains of Escherichia coli that carry the mutation uvrA6 show no measurable excision of pyrimidine dimers and are easily killed by ultraviolet (UV) light, whereas strains that carry recA13 are defective in genetic recombination and are also UV-sensitive. An Hfr strain carrying uvrA6 was crossed with an F− strain carrying recA13. Among the recombinants identified, one carrying uvrA recA proved to be of exceptional sensitivity to UV light. It is estimated from the UV dose (0.2 erg/mm2 at 253.7 nm) required to reduce the number of colony-forming cells by one natural logarithm that about 1.3 pyrimidine dimers were formed in a genome of 5 × 106 base pairs for each lethal event. This double mutant is 40 times more UV-sensitive than the excision-defective strain carrying uvrA6. The replication of one pyrimidine dimer is generally a lethal event in strains carrying recA13. Spontaneous breakdown and UV-induced breakdown of the deoxyribonucleic acid (DNA) of cells of the various genotypes were estimated by growing the cells in medium containing 3H-thymidine and measuring both acid-precipitable and acid-soluble radioactivity. The UV-induced degradation in strains with recA13 did not require the uvr+ genes and hence appears to depend upon a mechanism other than dimer excision. The greater level of survival after irradiation in Rec+ as compared to Rec− bacteria may be due to a recovery mechanism involving the reconstruction of the bacterial chromosome through genetic exchanges which occur between the newly replicated sister duplexes and which effectively circumvent the damaged bases remaining in the DNA.

Some properties of excision-defective recombination-deficient mutants of Escherichia coli K-12.

A method for obtaining by selection a certain class of sensitive mutants of Escherichia coli is reported. The method depends upon contra-selection by irradiated T1 bacteriophage. (auth)

/pdf/a-method-for-selecting-radiation-sensitive-mutants-of-54mnra6p4z.pdf

Lee Theriot

Papers

Mutants of escherichia coli k-12 defective in dna repair and in genetic recombination

Three loci in Escherichia coli K-12 that control the excision of pyrimidine dimers and certain other mutagen products from DNA.

A locus that controls filament formation and sensitivity to radiation in escherichia coli k-12.

Some properties of excision-defective recombination-deficient mutants of Escherichia coli K-12.

A method for selecting radiation-sensitive mutants of Escherichia coli.