Resistance and Cross-resistance of Escherichia coli Mutants to Antitumour Agent Mitomycin C

Greenberg, Joseph; Mandell, Joseph D.; Woody, Pearl L.

doi:10.1099/00221287-26-3-509

Cited by 30 publications

(17 citation statements)

References 12 publications

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“…Biochemical and genetic evidence suggest that the pathways which repair DNA damaged either by UV or by MC in Escherichia coli (3,38,44,45), Micrococcus radiodurans (33,34), and Bacillus subtilis (12) share at least some common gene functions. One consequence of overlapping repair pathways is that bacteria which are resistant to UV are often resistant to MC (3,14,33). Accordingly, we investigated whether such a positive correlation exists between UV and MC sensitivity among the Leptospira spp.…”

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Sensitivity of pathogenic and free-living Leptospira spp. to UV radiation and mitomycin C

Stamm

Charon

1988

Appl Environ Microbiol

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The habitats for the two major Leptospira spp. differ. The main habitat of L. biflexa is soil and water, whereas L. interrogans primarily resides in the renal tubules of animals. We investigated whether these two species, along with L. illini (species incertae sedis), differ with respect to their sensitivity to UV radiation. The doses of UV resulting in 37, 10, and 1 % survival were determined for representive serovars from each species. L. interrogans serovar pomona was 3.0 to 4.8 times more sensitive to UV than the other Leptospira species under the 37, 10, and 1% survival parameters. In comparison to other bacteria, L. interrogans serovar pomona is among the most sensitive to UV. In a qualitative UV sensitivity assay, L. interrogans serovars were found to be in general more sensitive than L. biflexa serovars. All three species were found to have a photoreactivation DNA repair mechanism. Since organisms that are resistant to UV are often resistant to the DNA cross-linking agent mitomycin C, we tested the relative sensitivity of several Leptospira serovars to this compound. With few exceptions, L. bifiexa and L. illini serovars were considerably more resistant to mitomycin C than the L. interrogans serovars. The mitomycin C sensitivity assay could be a useful addition to current characterization tests used to differentiate the Leptospira species.

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Sensitivity of pathogenic and free-living Leptospira spp. to UV radiation and mitomycin C

Stamm

Charon

1988

Appl Environ Microbiol

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“…It causes preferential inhibition of deoxyribonucleic acid (DNA) synthesis (22), degradation of DNA during post-treatment incubation (3,16,25), and induction of temperate phage (13,15,17). It also has a crossresistance relationship with UV irradiation (3,6,16). MTC is known to cause the formation in vivo and in vitro of a cross-linked DNA (9,10), whereas UV irradiation causes the formation of thymine dimers in DNA (4,21).…”

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Deoxyribonucleic Acid Damage by Monofunctional Mitomycins and Its Repair in Escherichia coli

Otsuji

Murayama

1972

J Bacteriol

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Exposure of Escherichia coli to the antibiotic mitomycin C (MTC) at a concentration of 0.5 ,ug/ml caused cross-linkage between complementary strands of deoxyribonucleic acid (DNA). Derivatives of mitomycin, 7-methoxymitosene (7-MMT) and decarbamoyl mitomycin C (DCMTC), at a level as high as 20 ,ug/ml formed no cross-links between DNA strands. Ultraviolet light-sensitive mutants of E. coli K-12 bearing uvrA, uvrB, uvrC, or recA mutations were more sensitive to the lethal action of 7-MMT and of DCMTC than was the wild-type strain. Treatment of wild-type cells with these antibiotics resulted in the production of single-strand breaks in DNA, which were repaired upon incubation in a growth medium. Such breaks in DNA were not produced in the uvrA and the uvrB mutants. In the uvrC mutant, single-strand breaks were produced by 7-MMT or by DCMTC, but these breaks were not repaired upon incubation. These results are discussed in connection with the mechanism for removal of pyrimidine dimers in ultraviolet-irradiated bacteria.

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“…Mutations that determine resistance to the mitomycins are chromosomally-localizable in B. subtilis and clustered in the early-replicating segment of the genome, which bears genetic loci for streptomycin and erythromycin resistance, and for ribosomal and transfer RNAs (IYER, 1966). Although the biochemical basis of mitomycin resistance is not known at present, the above results together with the known pleiotropic effects of mitomycin resistance (GREENBERG et al, 1961; lYER, 1966), and mitomycin effects on ribosomal function (SuzuKI and KILGORE, 1964), suggest that mitomycin resistance might be related to the latter function (IYER, 1966) or to some general permeability barriers. It might be of interest to mention a report by YosHIOKA and KuNII 220 W. SzYBALSKI and V. N. !YER: (1966}, who observed that mitomycin-resistant streptococcus mutants produced a mitomycin-inactivating factor.…”

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“…In the case of mitomycin-resistant E. coli, a lower degree of in vivo cross-linking was observed than in the corresponding sensitive mutant strains (IYER and SzYBALSKI, 1963). As discussed earlier, the cross resistance between mitomycin and radiation observed with some resistant strains (GREENBERG et al, 1961;GREENBERG and WOODY-KARRER, 1963) is most probably related to the similar repair mechanisms observed for UV or mitomycin damaged DNA (BoYcE and HowARD-FLANDERS, 1964;HowARD-FLANDERS et al, 1966). The temperature reactivation of mitomycin-exposed cells (WINKLER, 1962 a and b) could also be interpreted by involving the differential effect on the repair mechanism: temporary inhibition of DNA synthesis at high temperature permits the effective elimination of mitomycin-modified bases.…”

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confidence: 78%

Antibiotics

1967

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AII rights, especially that of tnmslation into foreign languages, reserved. It is also forbidden to reproduce this book, either whole DedicationFor most areas of scientific pursuit, there is usually that rare investigator who has the imagination to conceive ideas, who has faith in his visions, and who has the ability to critically test his concepts in the laboratory. Almost invariably, this scientist also inspires younger men to enthusiastically enter into his research program. To him should go the accolades and the recognitions of the esteem in which he is held. As only a small part of this esteem, we wish to dedicate these books to Professor SELMAN A. W AKSMAN in appreciation of his leadership and contributions in all facets of antibiotic research. PrefaceThe idea for publishing these books on the mechanism of action and on the biosynthesis of antibiotics was born of frustration in our attempts to keep abreast of the literature. Gone were the years when we were able to keep a bibliography on antibiotics and feel confident that we could find everything that was being published on this subject. These fields of investigation were moving forward so rapidly and were encompassing so wide a range of specialized areas in microbiology and chemistry that it was almost impossible to keep abreast of developments. In our naivete and enthusiasm, however, we were unaware that we were toying with an idea that might enmesh us, that we were creating an entity with a life of its own, that we were letting loose a Golom who instead of being our servant would be our master.That we set up ideals for these books is obvious; they would be current guides to developments and information in the areas of mechanism of action and biosynthesis of antibiotics. For almost every subject, we wished to enlist the aid of an investigator who himself had played a part in determining the nature of the phenomena that were being discussed. One concept for the books was that they include only antibiotics for which a definitive, well-documented mechanism of action or biosynthetic pathway was known. Yet, such an approach would not entirely serve the purpose we projected, for it would not encompass all of the information available in these fields of antibiotic investigations and blind searches for the original literature would still have to be made. We therefore chose to include any and all antibiotics about which some pertinent information had been published. It was obvious even at the start that such a compilation, integration, and analysis of information could never be complete unless scientific investigations ceased at the moment the last manuscript was submitted-an end that was neither desirable nor possible. An addendum was therefore included at the end of the volume and left open for the addition of new information until the last pages of the regular articles had been printed.The original concept has also been further expanded as the authors of several papers found it advisable to elaborate on their subject. Some of the articles included discussions...

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Resistance and Cross-resistance of Escherichia coli Mutants to Antitumour Agent Mitomycin C

Cited by 30 publications

References 12 publications

Sensitivity of pathogenic and free-living Leptospira spp. to UV radiation and mitomycin C

Sensitivity of pathogenic and free-living Leptospira spp. to UV radiation and mitomycin C

Deoxyribonucleic Acid Damage by Monofunctional Mitomycins and Its Repair in Escherichia coli

Antibiotics

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