rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
6
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pubmed:dateCreated |
1989-7-5
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pubmed:abstractText |
Plasmid recombination, like other homologous recombination in Escherichia coli, requires RecA protein in most conditions. We have found that the plasmid recombination defect in a recA mutant can be efficiently suppressed by the beta protein of bacteriophage lambda. beta protein is required for homologous recombination of lambda chromosomes during lytic phage growth in a recA host and is known to have a strand-annealing activity resembling that of RecA protein. The bioluminescence recombination assay was used for genetic analysis of beta-protein-mediated plasmid recombination. Efficient suppression of the recA mutation by beta protein required the absence of the E. coli nucleases exonuclease I and RecBCD nuclease. These nucleases inhibit a RecA-mediated plasmid recombination pathway that is more efficient than the pathway functioning in wild-type cells. Like RecA-mediated plasmid recombination in RecBCD- ExoI- cells, beta-protein-mediated plasmid recombination depended on concurrent DNA replication and on the activity of the recQ gene. However, unlike RecA-mediated plasmid recombination, beta-protein-mediated recombination in RecBCD- ExoI- cells was independent of recF and recJ activities. We propose that inactivation of exonuclease I and RecBCD nuclease stabilizes a recombination intermediate that is involved in RecA- and beta-protein-catalyzed homologous pairing reactions. We suggest that the intermediate may be linear plasmid DNA with a protruding 3' end, since these nucleases are known to interfere with the synthesis of such linear forms. The different recF and recJ requirements for beta-protein-dependent and RecA-dependent recombinations imply that the mechanisms of formation or processing of the putative intermediate differ in the two cases.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
IM
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pubmed:chemical |
|
pubmed:status |
MEDLINE
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pubmed:month |
Jun
|
pubmed:issn |
0021-9193
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pubmed:author |
|
pubmed:issnType |
Print
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pubmed:volume |
171
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
|
pubmed:pagination |
3523-9
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:2542228-Bacterial Proteins,
pubmed-meshheading:2542228-Bacteriophage lambda,
pubmed-meshheading:2542228-Escherichia coli,
pubmed-meshheading:2542228-Exodeoxyribonucleases,
pubmed-meshheading:2542228-Genes, Bacterial,
pubmed-meshheading:2542228-Luciferases,
pubmed-meshheading:2542228-Plasmids,
pubmed-meshheading:2542228-Rec A Recombinases,
pubmed-meshheading:2542228-Recombination, Genetic,
pubmed-meshheading:2542228-Suppression, Genetic,
pubmed-meshheading:2542228-Viral Proteins
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pubmed:year |
1989
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pubmed:articleTitle |
Suppression of recA deficiency in plasmid recombination by bacteriophage lambda beta protein in RecBCD- ExoI- Escherichia coli cells.
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pubmed:affiliation |
Department of Molecular Genetics, Hebrew University-Hadassah Medical School, Jerusalem, Israel.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|