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Proc Natl Acad Sci U S A. 1970 July; 66(3): 587–594.
PMCID: PMC283090
Bacteriophage Lambda; Abortive Infection of Bacteria Lysogenic for Phage P2*
Gunnar Lindahl, Gianpiero Sironi, Harvey Bialy, and Richard Calendar§
DEPARTMENT OF MICROBIAL GENETICS, KAROLINSKA INSTITUTET, STOCKHOLM, SWEDEN
DEPARTMENT OF MOLECULAR BIOLOGY, UNIVERSITY OF CALIFORNIA (BERKELEY)
Present address: Laboratoire de Génétique Cellulaire Institut Pasteur, 25, Rue de Docteur Roux, Paris XV, France.
Present address: Istituto di Genetica, Universita di Milano, Via Celoria 10, Milan, Italy 20133.
§ Requests for reprints may be addressed to Dr. R. Calendar, Department of Molecular Biology, University of California, Berkeley, Calif. 94720.
* This investigation was supported in part by U.S. Public Health Research grants AI 01267 and AI 08722 from the Institute of Allergy and Infectious Diseases, by training grant GM 01389 from the Institute of General Medical Sciences, and by a Biomedical Sciences Support grant FR-7006 from the General Research Support Branch, Division of Research Resources, Bureau of Health Professions Education and Manpower Training, National Institutes of Health. Aided by a joint grant from the Swedish Medical and Natural Science Research Councils and the Swedish Cancer Society; by grant IN-87C from the American Cancer Society, and by grant N.115.2351.0.4283 from the Italian Centro Nazionale delle Ricerche.
Abstract
The efficiency of plating of wild-type λ on a host lysogenic for P2 is less than 10-6, and only a small number of infected cells produce progeny phage. Lambda can adsorb and inject its DNA normally in such cells; the DNA can circularize and is not nicked or degraded, but replication is severely impaired. Mutants of P2, which as prophages no longer interfere with λ, have been isolated and found to be recessive to wild type, implying that P2 prophage codes for a diffusible product involved in λ interference. The P2 gene product responsible for preventing λ growth also kills recombination-deficient bacteria of the recB and recC classes under conditions where P2 does not normally kill the host. Mutants of λ that are resistant to interference are recessive to wild-type λ. Thus λ actively participates in its own interference. The λ-mutants that are resistant to interference are unable to synthesize at least two nonessential proteins. In addition, they are unable to grow on recombination-deficient bacteria of the recA class, but they can grow on recA recB double mutants.
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Selected References
These references are in PubMed. This may not be the complete list of references from this article.
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