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  • 1
    Electronic Resource
    Electronic Resource
    [s.l.] : Nature Publishing Group
    Nature structural & molecular biology 12 (2005), S. 215-216 
    ISSN: 1545-9985
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] The SOS response to DNA damage in Escherichia coli, which was discovered over 30 years ago, involves the coordinated expression of at least 43 genes. Under noninducing conditions, the LexA protein binds to the operator of each of the SOS-inducible genes, and to its own operator, repressing ...
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1203
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Werner syndrome (WS) is a rare autosomal recessive disorder of humans characterized by the premature onset and accelerated rate of development of several major age-related disorders. An aberration in DNA replication or repair is suggested by the evidence of genome instability. Since the structural gene for DNA polymerase β maps within the region of the WS mutation on the short arm of chromosome 8 and is involved in both DNA repair and DNA replication, we evaluated its candidacy as the WS gene. Several independent lines of evidence did not support that hypothesis: (1) activity gels showed normal enzyme activity and electrophoretic mobility; (2) nucleotide sequence analysis of the entire coding region failed to reveal mutations (although indicated mistakes in the published sequence); (3) single-strand conformation polymorphism (SSCP) and heteroduplex analyses failed to reveal evidence of mutations in the promoter region; (4) a newly discerned polymorphism failed to reveal evidence of homozygosity by descent in a consanguineous patient; and 5) fluorescence in situ hybridization (FISH) analysis placed the DNA polymerase β gene centromeric to D8S135 at 8p11.2 and thus beyond the region of peak LOD scores for WS.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Molecular genetics and genomics 248 (1995), S. 217-224 
    ISSN: 1617-4623
    Keywords: Polymeraseβ ; DNA replication DNA repair ; Mutagenesis ; RecA protein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract We used quantitative complementation assays to characterize individual DNA polymeraseβ (Polβ) mutants for their ability to function in DNA replication and DNA repair. We also describe a screen for detecting imitator activity of DNA polymeraseβ mutants. By using these bioassays, together with DNA polymerase activity gels, we characterized 15 new DNA polymeraseβ mutants that display a wide spectrum of phenotypes. Most of these mutants are generally defective in their ability to synthesize DNA. However, two of our Polβ mutants show more complex phenotypes: they are able to function in DNA repair but unable to participate in DNA replication. One of our mutants displays imitator activity in vivo. Our work provides a model to study mutant mammalian enzymes inEscherichia coli with phenotypes that are otherwise difficult to assess.
    Type of Medium: Electronic Resource
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