Affiliation:
1. Department of Bacterial Immunology, Walter Reed Army Institute of Research, Washington, D.C. 20012
Abstract
The insensitivity of wild-type
Shigella flexneri
2a to coliphage λ is a consequence of its native genetic defect in the
malA
gene cluster. The “smooth”
S. flexneri
2a lipopolysaccharide layer affects the efficient adsorption of λ. Derivatives, capable of serving as functional hosts for λ, were obtained by repairing the
malA
lesion, enabling the expression of the
malB
-λ
rcp
region of
S. flexneri.
Introduction of a mutation into
S. flexneri
causing a “rough” lipopolysaccharide character resulted in more efficient adsorption of λ. Such
S. flexneri
hosts can be stably lysogenized and upon induction yield
gal
+
-transducing lysates. Lambda propagated on a
malA
+
rough
S. flexneri
host was restricted by
Escherichia coli
K-12 and
E. coli
B, but not by
E. coli
C. This
S. flexneri
host did not restrict λ grown on these
E. coli
strains.
Publisher
American Society for Microbiology
Subject
Virology,Insect Science,Immunology,Microbiology
Cited by
12 articles.
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