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Chromosomal Aberrations Associated with Mutations to Bacteriophage Resistance in Escherichia coli

Chromosomal Aberrations Associated with Mutations to Bacteriophage Resistance in Escherichia coli Chromosomal Aberrations Associated with Mutations to Bacteriophage Resistance in Escherichia coli ABSTRACT Curtiss, Roy , III (University of Chicago, Chicago, Ill., and Oak Ridge National Laboratory, Oak Ridge, Tenn.). Chromosomal aberrations associated with mutations to bacteriophage resistance in Escherichia coli . J. Bacteriol. 89: 28–40. 1965.—Ten types of mutants of Escherichia coli K-12 resistant to bacteriophage T 3 have been isolated, and several of these types have been studied genetically. Many of the / 3,4,7 , / 3,4,7 ,λ, and / 3,4,7 ,λ, pro − 1,2 mutants were unstable, changing to complete sensitivity to T 4 . The results with strains having / 3,4,7 ,λ, pro − 1,2 mutations were compatible with the hypothesis that this mutation caused a single break in the circular chromosome which prevented the normal association in the inheritance of the outside markers leu + and lac + . When sensitivity to T 4 was regained, association in the inheritance of outside markers was restored, and the resulting / 3,7 ,λ, pro − 1,2 mutation behaved genetically as a deletion. The / 3,7 ,λ, pro − 1,2 and / 3,4,7 ,λ, pro − 1,2 mutations caused positive interference, inhibition of genetic recombination in regions adjacent to them, and the formation of unstable partial diploid recombinants. One group of / 3,4,7 ,λ mutations did not occur in the leu to try region of the bacterial genome. Other / 3,4,7 ,λ mutations in F − bacteria prevented the joint inheritance of the outside markers lac + and gal + , presumably by breakage of the circular chromosome. Hfr and F + strains with / 3,4,7 ,λ mutations at this locus were unable to conjugate; therefore, a complete genetic analysis of the effects of this / 3,4,7 ,λ mutation could not be done. Roy Curtiss III 1 a Department of Microbiology, University of Chicago, Chicago, Illinois, and Biology Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Bacteriology American Society For Microbiology

Chromosomal Aberrations Associated with Mutations to Bacteriophage Resistance in Escherichia coli

Journal of Bacteriology , Volume 89 (1): 28 – Jan 1, 1965

Chromosomal Aberrations Associated with Mutations to Bacteriophage Resistance in Escherichia coli

Journal of Bacteriology , Volume 89 (1): 28 – Jan 1, 1965

Abstract

Chromosomal Aberrations Associated with Mutations to Bacteriophage Resistance in Escherichia coli ABSTRACT Curtiss, Roy , III (University of Chicago, Chicago, Ill., and Oak Ridge National Laboratory, Oak Ridge, Tenn.). Chromosomal aberrations associated with mutations to bacteriophage resistance in Escherichia coli . J. Bacteriol. 89: 28–40. 1965.—Ten types of mutants of Escherichia coli K-12 resistant to bacteriophage T 3 have been isolated, and several of these types have been studied genetically. Many of the / 3,4,7 , / 3,4,7 ,λ, and / 3,4,7 ,λ, pro − 1,2 mutants were unstable, changing to complete sensitivity to T 4 . The results with strains having / 3,4,7 ,λ, pro − 1,2 mutations were compatible with the hypothesis that this mutation caused a single break in the circular chromosome which prevented the normal association in the inheritance of the outside markers leu + and lac + . When sensitivity to T 4 was regained, association in the inheritance of outside markers was restored, and the resulting / 3,7 ,λ, pro − 1,2 mutation behaved genetically as a deletion. The / 3,7 ,λ, pro − 1,2 and / 3,4,7 ,λ, pro − 1,2 mutations caused positive interference, inhibition of genetic recombination in regions adjacent to them, and the formation of unstable partial diploid recombinants. One group of / 3,4,7 ,λ mutations did not occur in the leu to try region of the bacterial genome. Other / 3,4,7 ,λ mutations in F − bacteria prevented the joint inheritance of the outside markers lac + and gal + , presumably by breakage of the circular chromosome. Hfr and F + strains with / 3,4,7 ,λ mutations at this locus were unable to conjugate; therefore, a complete genetic analysis of the effects of this / 3,4,7 ,λ mutation could not be done. Roy Curtiss III 1 a Department of Microbiology, University of Chicago, Chicago, Illinois, and Biology Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee

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Publisher
American Society For Microbiology
Copyright
Copyright © 1965 by the American society for Microbiology.
ISSN
0021-9193
eISSN
1098-5530
Publisher site
See Article on Publisher Site

Abstract

Chromosomal Aberrations Associated with Mutations to Bacteriophage Resistance in Escherichia coli ABSTRACT Curtiss, Roy , III (University of Chicago, Chicago, Ill., and Oak Ridge National Laboratory, Oak Ridge, Tenn.). Chromosomal aberrations associated with mutations to bacteriophage resistance in Escherichia coli . J. Bacteriol. 89: 28–40. 1965.—Ten types of mutants of Escherichia coli K-12 resistant to bacteriophage T 3 have been isolated, and several of these types have been studied genetically. Many of the / 3,4,7 , / 3,4,7 ,λ, and / 3,4,7 ,λ, pro − 1,2 mutants were unstable, changing to complete sensitivity to T 4 . The results with strains having / 3,4,7 ,λ, pro − 1,2 mutations were compatible with the hypothesis that this mutation caused a single break in the circular chromosome which prevented the normal association in the inheritance of the outside markers leu + and lac + . When sensitivity to T 4 was regained, association in the inheritance of outside markers was restored, and the resulting / 3,7 ,λ, pro − 1,2 mutation behaved genetically as a deletion. The / 3,7 ,λ, pro − 1,2 and / 3,4,7 ,λ, pro − 1,2 mutations caused positive interference, inhibition of genetic recombination in regions adjacent to them, and the formation of unstable partial diploid recombinants. One group of / 3,4,7 ,λ mutations did not occur in the leu to try region of the bacterial genome. Other / 3,4,7 ,λ mutations in F − bacteria prevented the joint inheritance of the outside markers lac + and gal + , presumably by breakage of the circular chromosome. Hfr and F + strains with / 3,4,7 ,λ mutations at this locus were unable to conjugate; therefore, a complete genetic analysis of the effects of this / 3,4,7 ,λ mutation could not be done. Roy Curtiss III 1 a Department of Microbiology, University of Chicago, Chicago, Illinois, and Biology Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee

Journal

Journal of BacteriologyAmerican Society For Microbiology

Published: Jan 1, 1965

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