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!align=left  |Citation
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'''Hochhauser, SJ and Weiss, B'''  (1978) Escherichia coli mutants deficient in deoxyuridine triphosphatase. ''J. Bacteriol.'' '''134''':157-66
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!align=left  |Abstract
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Mutants deficient in deoxyuridine triphosphatase (dUTPase) were identified by enzyme assays of randomly chosen heavily mutagenized clones. Five mutants of independent origin were obtained. One mutant produced a thermolabile enzyme, and it was presumed to have a mutation in the structural gene for dUTPase, designated dut. The most deficient mutant had the following associated phenotypes: less than 1% of parental dUTPase activity, prolonged generation time, increased sensitivity to 5'-fluorodeoxyuridine, increased rate of spontaneous mutation, increased rate of recombination (hyper-Rec), an inhibition of growth in the presence of 2 mM uracil, and a decreased ability to support the growth of phage P1 (but not T4 or lambda). This mutation also appeared to be incompatible with pyrE mutations. A revertant selected by its faster growth had regained dUTPase activity and lost its hyper-Rec phenotype. Many of the properties of the dut mutants are compatible with their presumed increased incorporation of uracil into DNA and the subsequent transient breakage of the DNA by excision repair.
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[http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=148458 PubMed] [http://www.ncbi.nlm.nih.gov/pmc/articles/PMC222230 PMC222230]
 
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!align=left  |Keywords
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Coliphages/genetics; Coliphages/growth & development; Deoxyuracil Nucleotides; Escherichia coli/enzymology; Escherichia coli/genetics; Floxuridine/pharmacology; Genes; Genetic Linkage; Mutation; Pyrophosphatases/biosynthesis; Recombination, Genetic; Transduction, Genetic; Uracil/pharmacology
 
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==See also==
 
==References==
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Latest revision as of 06:37, 13 November 2014

Citation

Hochhauser, SJ and Weiss, B (1978) Escherichia coli mutants deficient in deoxyuridine triphosphatase. J. Bacteriol. 134:157-66

Abstract

Mutants deficient in deoxyuridine triphosphatase (dUTPase) were identified by enzyme assays of randomly chosen heavily mutagenized clones. Five mutants of independent origin were obtained. One mutant produced a thermolabile enzyme, and it was presumed to have a mutation in the structural gene for dUTPase, designated dut. The most deficient mutant had the following associated phenotypes: less than 1% of parental dUTPase activity, prolonged generation time, increased sensitivity to 5'-fluorodeoxyuridine, increased rate of spontaneous mutation, increased rate of recombination (hyper-Rec), an inhibition of growth in the presence of 2 mM uracil, and a decreased ability to support the growth of phage P1 (but not T4 or lambda). This mutation also appeared to be incompatible with pyrE mutations. A revertant selected by its faster growth had regained dUTPase activity and lost its hyper-Rec phenotype. Many of the properties of the dut mutants are compatible with their presumed increased incorporation of uracil into DNA and the subsequent transient breakage of the DNA by excision repair.

Links

PubMed PMC222230

Keywords

Coliphages/genetics; Coliphages/growth & development; Deoxyuracil Nucleotides; Escherichia coli/enzymology; Escherichia coli/genetics; Floxuridine/pharmacology; Genes; Genetic Linkage; Mutation; Pyrophosphatases/biosynthesis; Recombination, Genetic; Transduction, Genetic; Uracil/pharmacology

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