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  • 1
    Electronic Resource
    Electronic Resource
    Osney Mead, Oxford OX2 0EL, UK : Blackwell Science Ltd
    Molecular microbiology 18 (1995), S. 0 
    ISSN: 1365-2958
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Expression of the lactose operon upon induction by IPTG was studied with Escherichia coli B/r and K-12 strains as a function of exposure to ultraviolet light. Patterns of expression inactivation were compared in cells with wild-type UvrABC nucleotide excision repair, with transcription-coupled excision repair (TCR) specifically defective because of a defect at mfd, or with excision repair (ER) and TCR eliminated by defects at uvrA or uvrC. Sets of inactivation patterns were also determined for cells expressing the lactose operon via the ‘UV5’ promoter, an alternative to the wild-type promoter that eliminates dependence of expression on negative DNA supercoiling. The results demonstrated a major contribution by TCR to successful gene expression. Gene expression was more sensitive to u.v. inactivation when TCR was defective and similarly more sensitive when both ER and TCR were defective. Thus, TCR may be the only means of repairing transcription-blocking damage at active genes. Contrasting results with wild-type and UV5 promoters suggested that relaxed supercoiling might accompany repair and reduce expression even though a template lesion is removed. A test of mismatch repair defects on ultraviolet inactivation of gene expression found only limited interference with TCR as it benefits gene expression.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 249 (1995), S. 585-590 
    ISSN: 1617-4623
    Keywords: UV mutagenesis ; Excision repair ; Mismatch repair
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Mutation frequency decline (MFD) in Escherichia coli was examined for effects associated with genetic defects in mismatch repair. The kinetics of MFD are slower when the B/r strain WU3610 carries the mutation mutS201::Tn5 or mutL::Tn10, both of which affect mismatch repair. Similar slow kinetics are produced by mutH34 but not by mutH471::Tn5; the latter has no apparent effect. Strain WU3610-45 (mfd-1) produces the slower kinetics if transcription is inhibited during the post-UV incubation, although it produces no decline in normal circumstances. The slower kinetics are therefore attributed to bulk excision repair that remains when rapid transcription-coupled repair (TCR) is eliminated by certain defects in mismatch repair. A model is proposed wherein mismatch repair defects are thought to slow the activity of TCR but, unlike an mfd defect, not to impede dissociation of stalled transcription complexes at lesions in the transcribed DNA strand.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 249 (1995), S. 591-599 
    ISSN: 1617-4623
    Keywords: Targeted mutagenesis ; Excision repair ; Cyclobutane pyrimidine dimers ; Cytosine deamination
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Mutation frequency decline (MFD) in Escherichia coli was examined to demonstrate repair of targeting photoproducts during the post-UV incubation required in this process. Repair of mutation-targeting cyclobutane pyrimidine dimers (T 〈〉 C) was demonstrated when a correlation was established between the mutation frequency normally associated with these lesions and the rate of mutation production at these lesions by spontaneous deamination of cytosines and photoreversal in ung-defective cells. An incubation producing a decline in mutation frequency, i.e., MFD, also produces lower rates of mutation increase via the deamination mechanism. Since the latter assay involves processes entirely within the post-UV incubation period, the lower rates are attributed to rapid transcription-coupled nucleotide excision repair (TCR) that reduces the number of relevant T 〈〉 C dimers during this period. Rediscovery of the neglected fact that MFD can be stimulated by post-UV incubation in buffer alone is part of the analysis. Results presented here and a variety of others are discussed to support a model of MFD as a particular example of TCR: effective repair of photoproducts in the transcribed DNA strand that target glutamine tRNA suppressor mutations occurs during the appropriate post-UV incubation and is responsible for MFD.
    Type of Medium: Electronic Resource
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