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Journal of Bacteriology, February 1999, p. 1352-1355, Vol. 181, No. 4
Department of Molecular Biology and
Microbiology, Tufts University Medical School, Boston,
Massachusetts 02111-1800,1 and
Sackler
Laboratory of Molecular Genetics and Informatics, Rockefeller
University, New York, New York 10021-63992
Received 24 June 1996/Accepted 7 February 1997
The T4 head protein, gp2, promotes head-tail joining during phage
morphogenesis and is also incorporated into the phage head. It protects
the injected DNA from degradation by exonuclease V during the
subsequent infection. In this study, we show that recombinant gp2, a
very basic protein, rapidly kills the cells in which it is expressed.
To further illustrate the protectiveness of gp2 for DNA termini, we
compare the effect of gp2 expression on Red-mediated and
Int-mediated recombination. Red-mediated recombination is nonspecific
and requires the transient formation of double-stranded DNA termini.
Int-mediated recombination, on the other hand, is site specific and
does not require chromosomal termini. Red-mediated recombination is
inhibited to a much greater extent than is Int-mediated recombination.
We conclude from the results of these physiological and genetic
experiments that T4 gp2 expression, like Mu Gam expression, kills
bacteria by binding to double-stranded DNA termini, the most likely
mode for its protection of entering phage DNA from exonuclease V.
0021-9193/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
Bacteriophage T4 gp2 Interferes with Cell Viability
and with Bacteriophage Lambda Red Recombination

*
Corresponding author. Mailing address: Department of
Molecular Biology and Microbiology, Tufts University Medical School, Boston, MA 02111-1800. Phone: (617) 636-6754. Fax: (617) 636-0337. E-mail: egoldber{at}opal.tufts.edu.
Present address: Department of Surgery, Brigham and Women's
Hospital, Harvard Medical School, Boston, MA 02115.
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