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  • 1
    Electronic Resource
    Electronic Resource
    Palo Alto, Calif. : Annual Reviews
    Annual Review of Biochemistry 48 (1979), S. 783-836 
    ISSN: 0066-4154
    Source: Annual Reviews Electronic Back Volume Collection 1932-2001ff
    Topics: Chemistry and Pharmacology , Biology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 214 (1967), S. 269-270 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Cultures of E. coli strain TAU-bar were grown as previously described9 on a glucose-salts medium with the required supplements (thymine, uracil, arginine proline, methionine, and tryptophan). The cells were allowed to complete the normal DNA replication cycle in conditions of amino-acid ...
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature 198 (1963), S. 286-286 
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Our previous work with strain TA U has indicated that uracil deficiency does not prevent thymineless killing2. However, this strain is known to be able to synthesize up to 2 per cent of its uracil requirement5. Also, TAU succumbs to thymine deprivation in a phosphate-deficient medium6, as ...
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Archives of dermatological research 279 (1987), S. 147-150 
    ISSN: 1432-069X
    Keywords: Psoriasis ; Nalidixic acid ; Novobiocin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Our studies in human epidermal keratinocytes as a model system have suggested that the antibiotic topoisomerase II inhibitors, novobiocin and nalidixic acid, may be of value for the treatment of hyperproliferative skin disorders. We have therefore conducted a pilot study of the clinical efficacy of these compounds for the treatment of psoriasis. The compounds were administered topically to psoriatic plaques in seven healthy patients over a period of 6 weeks. Nalidixic acid (2%) or novobiocin (2% or 5%) in methylcellulose were applied twice daily under occlusion, and methylcellulose alone was used as a control. In six of the seven patients, one or both compounds effected somewhat greater improvement than in the control within 3 weeks of treatment.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 150 (1977), S. 237-248 
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Certain treatments that damage DNA and/or inhibit replication in E. coli have been reported to induce synthesis of a new protein, termed protein X, in recA + lexA + strains. We have examined some of the treatments that might induce protein X and we have, in particular, tested the hypothesis of Gudas and Pardee (1975) that DNA degradation products play an essential role in the induction process. We confirmed that UV irradiation, nalidixic acid treatment, or thymine starvation result in protein X synthesis in wild type strains. However, we found that UV irradiation, unlike nalidixic acid, also induced protein X in recB strains, in which little DNA degradation occurs. Furthermore, we found that the presence of DNA fragments resulting from host-controlled restriction of phage λ DNA did not affect protein X synthesis. We conclude that no causal relationship exists between the production of DNA fragments and induction of protein X. The presence of the plasmid R46, which confers enhanced mutagenesis and UV resistance on its host, did not affect protein X synthesis. Growth in the presence of 5-bromouracil, which does not result in production of degradation fragments, resulted eventually in a low rate of protein X synthesis. In dnaA mutants, deficient in the initiation of new rounds of replication, UV irradiation induced protein X, again unlike nalidixic acid. Thus, the inhibition of active replication forks is not an essential requirement for protein X induction.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 101 (1968), S. 191-202 
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary 1. Two mutant strains have been derived from Escherichia coli TAU-bar; one selected for resistance to nitrosoguanidine at pH 7.5 and the other for resistance to diazomethane. The comparative study of these strains shows that diazomethane, a decomposition product of nitrosoguanidine, is the principal agent involved in both lethal and mutagenic effects of nitrosoguanidine above pH 5. Nitrosoguanidine is the lethal agent at pH 5 and it is possibly a lesser mutagen itself. 2. There are two types of chromosomal effects, lethal (susceptible to repair replication) and mutagenic (non-repairable), both due mostly to diazomethane. 3. The expression of mutations was found to be independent of DNA replication or repair. The optimal conditions for nitrosoguanidine mutagenesis are discussed.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 262 (1999), S. 543-551 
    ISSN: 1617-4623
    Keywords: Key words Replication ; DNA repair ; recJ ; recQ ; UV irradiation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The accurate recovery of replication following DNA damage and repair is critical for the maintenance of genomic integrity. In Escherichia coli, the recovery of replication following UV-induced DNA damage is dependent upon several proteins in the recF pathway, including RecF, RecO, and RecR. Two other recF pathway proteins, the RecQ helicase and the RecJ exonuclease, have been shown to affect the sites and frequencies at which illegitimate rearrangements occur following UV-induced DNA damage, suggesting that they also may function during the recovery of replication. We show here that RecQ and RecJ process the nascent DNA at blocked replication forks prior to the resumption of DNA synthesis. The processing involves selective degradation of the nascent lagging DNA strand and it requires both RecQ and RecJ. We suggest that this processing may serve to lengthen the substrate that can be recognized and stabilized by the RecA protein at the replication fork, thereby helping to ensure the accurate recovery of replication after the obstructing lesion has been repaired.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 255 (1997), S. 449-459 
    ISSN: 1617-4623
    Keywords: Key words MutS ; Mutation frequency variation ; Preferential mutagenesis ; Directed mutagenesis ; Mismatch repair
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract To study the variation in spontaneous mutation frequencies in different chromosomal domains, a mini-Mu-kan-lacZ −transposable element was constructed to insert the lacZ −(Trp570 → Opal) allele into many different loci in the Escherichia coli chromosome. Papillation on MacConkey lactose plates was used to screen for mini-Mu insertion mutants with elevated levels of spontaneous mutagenesis of lacZop → LacZ+ candidates were then screened for normal mutation frequencies in other genes. Two different insertion mutants with this enhanced mutagenesis phenotype were isolated from 14 000 colonies, and named plm-1 (preferential lacZmutagenesis) and plm-2. The frequency of LacZ−→ LacZ+ mutations in these plm mutants was over 400-fold higher than that in isogenic strains containing mini-Mu-kan-lacZop insertions at other loci. Six Lac+ reversion (or suppression) mutations obtained from each of the two plm mutants were mapped by P1 transduction and all were found to be linked to the Kanr gene in the mini-Mu-kan-lacZop, suggesting that a localized mutagenic event is responsible for the preferential mutagenesis. Furthermore, both the LacZ+→ LacZ−and Kanr→ Kans mutant frequencies of these Lac+ revertants were in the range of 10−3 to 10−2, indicating that this putative localized mutagenesis is neither allele nor gene specific. To identify the plm loci, the chromosomal regions flanking the mini-Mu insertion sites were cloned and sequenced. A computer-assisted database search of homologous sequences revealed that the plm-1 locus is identical to the mutS gene; the mini-Mu insertion most probably results in the production of a truncated MutS protein. We suggest that the enhanced lacZ mutation frequency in plm-1 may be associated with an active process involving the putative truncated MutS protein. The DNA sequence of the plm-2 locus matched a putative malate oxidoreductase gene located at 55.5 min of the E. coli chromosome.
    Type of Medium: Electronic Resource
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