Isolation and characterization of mutants of Escherichia coli deficient in induction of mutations by ultraviolet light

Kato, Takao; Shinoura, Yukiko

doi:10.1007/bf00283484

Cited by 561 publications

(319 citation statements)

References 37 publications

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“…Three chromosomal missense umuC mutants have been reported (28,31,48), and we were interested in comparing the effects of the chromosomal mutants in our plasmid expression system. Neither umuC36 nor umuC104 promoted any significant spontaneous mutator activity; however, both exhibited a very limited ability to promote MMS-induced mutagenesis in (Table 3).…”

Section: Resultsmentioning

confidence: 99%

“…To some extent this is due to the limited number of umuC mutants that have been characterized genetically. The E. coli umuC gene consists of 1,269 base pairs, and to date, only eight umuC mutants have been reported: four missense mutants (three chromosomal and one plasmid) (28,31,36,48), two frameshift mutants that result in nonsense mutations (both plasmid encoded) (41), and two insertional mutants (both chromosomal) (1,16).…”

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confidence: 99%

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Isolation and characterization of novel plasmid-encoded umuC mutants

Woodgate¹,

Singh²,

Kulaeva³

et al. 1994

J Bacteriol

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Interestingly, these plasmid mutants fell into two classes: (i) 5 were expression mutants that produced either too little or too much wild-type UmuC protein, and (ii) 11 were plasmids with structural changes in the UmuC protein. Although hydroxylamine mutagenesis was random, most of the structural mutants identified in the screen were localized to two regions of the UmuC protein; four mutations were found in a stretch of 30 amino acids (residues 133 to 162) in the middle of the protein, while four other mutations (three of which resulted in a truncated UmuC protein) were localized in the last 50 carboxyl-terminal amino acid residues. These new plasmid umuC mutants, together with the previously identified chromosomal umuC25, umuC36, and umuC104 mutations that we have also cloned, should prove extremel useful in dissecting the genetic and biochemical activities of UmuC in mutagenic DNA repair.

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

Isolation and characterization of novel plasmid-encoded umuC mutants

Woodgate¹,

Singh²,

Kulaeva³

et al. 1994

J Bacteriol

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“…Moreover, frameshift mutations frequently occur at high frequencies within specific sequence contexts, known as mutation hot spots thus leaving a strong mutagenic imprint (Fuchs et al, 1981). Genetic studies identified loci such as the umuDC operon (Kato and Shinoura, 1977;Steinborn, 1978) in E. coli and the various REV genes (Lemontt, 1971) in S. cerevisiae which abolish induced mutagenesis when mutated. It therefore became clear that mutagenesis was an active process involving specific proteins in addition to the replicative DNA polymerase.…”

Section: Introductionmentioning

confidence: 99%

How DNA lesions are turned into mutations within cells?

2002

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Genomes of all living organisms are constantly injured by endogenous and exogenous agents that modify the chemical integrity of DNA and in turn challenge its informational content. Despite the efficient action of numerous repair systems that remove lesions in DNA in an error-free manner, some lesions, that escape these repair mechanisms, are present when DNA is being replicated. Although replicative DNA polymerases are usually unable to copy past such lesions, it was recently discovered that cells are equipped with specialized DNA polymerases that will assist the replicative polymerase during the process of Translesion Synthesis (TLS). These TLS polymerases exhibit relaxed fidelity that allows them to copy past lesions in DNA with an inherent risk of generating mutations at high frequency. We present recent aspects related to the genetics and biochemistry of TLS and highlight some of the remaining hot topics of this field.

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“…This global stress response initially induces enzymes that function in the high fidelity modes of excision and recombinational repair; however, when damage is too extensive to be corrected by such conventional means, a mutagenic process is activated that permits replicative synthesis past lesions but in an error-prone manner (3). The products of the umuC and umuD genes are essential to this translesion synthesis (4,5). Although DNA polymerase III itself is capable of some misincorporation (6), the UmuC and UmuDЈ proteins facilitate continued extension from the mispaired base (7), and very recent data suggest that UmuC and UmuDЈ proteins directly affect nucleotide mis-insertion (8) as well.…”

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confidence: 99%

Modulation of RecA Nucleoprotein Function by the Mutagenic UmuD′C Protein Complex

Rehrauer¹,

Bruck²,

Woodgate³

et al. 1998

Journal of Biological Chemistry

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The RecA, UmuC, and UmuD proteins are essential for error-prone, replicative bypass of DNA lesions. Normally, RecA protein mediates homologous pairing of DNA. We show that purified Umu(D) 2 C blocks this recombination function. Biosensor measurements establish that the mutagenic complex binds to the RecA nucleoprotein filament with a stoichiometry of one Umu(D) 2 C complex for every two RecA monomers. Furthermore, Umu(D) 2 C competitively inhibits LexA repressor cleavage but not ATPase activity, implying that Umu(D) 2 C binds in or proximal to the helical groove of the RecA nucleoprotein filament. This binding reduces joint molecule formation and even more severely impedes DNA heteroduplex formation by RecA protein, ultimately blocking all DNA pairing activity and thereby abridging participation in recombination function. Thus, Umu(D) 2 C restricts the activities of the RecA nucleoprotein filament and presumably, in this manner, recruits it for mutagenic repair function. This modulation by Umu(D) 2 C is envisioned as a key event in the transition from a normal mode of genomic maintenance by "error-free" recombinational repair, to one of "errorprone" DNA replication.

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Isolation and characterization of mutants of Escherichia coli deficient in induction of mutations by ultraviolet light

Cited by 561 publications

References 37 publications

Isolation and characterization of novel plasmid-encoded umuC mutants

Isolation and characterization of novel plasmid-encoded umuC mutants

How DNA lesions are turned into mutations within cells?

Modulation of RecA Nucleoprotein Function by the Mutagenic UmuD′C Protein Complex

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