1 Department of Bacterial Immunology, Division of Communicable Diseases and Immunology, Walter Reed Army Institute of Research, Washington, D.C. 20012
ABSTRACT
Hybrids between Escherichia coli K-12 and Salmonella typhosa which conserved a continuous K-12 chromosomal diploid segment extending from pro through ara to the strA locus were sensitive to plaque formation by wild-type
. These partially diploid S. typhosa hybrids could be lysogenized with
and subsequently induced to produce infectious phage particles. When the K-12 genes were segregated from a lysogenic S. typhosa hybrid, phage-productive ability was no longer detectable due to loss of a genetic region necessary for vegetative replication of
. However,
prophage was shown to persist in a quiescent state in the S. typhosa hybrid segregant with phage-productive ability being reactivated after replacement of the essential K-12
replication region. Low-frequency transduction and high-frequency transduction lysates containing the gal+ genes of S. typhosa were prepared by induction of
-lysogenic S. typhosa hybrids indicating that the att
site is chromosomally located in S. typhosa in close proximity to the gal locus as in E. coli K-12. After propagation in S. typhosa hybrids,
was subject to restriction by E. coli K-12 recipients, thus establishing that S. typhosa does not perform the K-12 modification of
deoxyribonucleic acid. Hybrids of S. typhosa, however, did not restrict
grown previously on E. coli K-12. The K-12 genetic region required for
phage production in S. typhosa was located within min 66 to min 72 on the genetic map of the E. coli chromosome. Transfer of an F-merogenote encompassing the 66 to 72 min E. coli chromosomal region to
-insensitive S. typhosa hybrids enabled them to replicate wild-type
. The
-insensitive S. typhosa hybrid, WR4255, which blocks
replication, can be mutagenized to yield mutant strains sensitive to
vir and
imm434. These WR4255 mutants remained insensitive to plaque formation by wild-type
.
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