Constitutive λ DNA replication by λc17, a regulatory mutant related to virulence

doi:10.1016/0042-6822(68)90099-8

Virology

Volume 34, Issue 4, April 1968, Pages 778-789

https://doi.org/10.1016/0042-6822(68)90099-8 Get rights and content

Abstract

λc₁₇ is a mutant of λ originally recognized by Pereira da Silva because of its nearly clear plaque morphology on a sensitive host and its ability to give virulence when combined in cis with certain cI mutations. Experiments are presented which show that c₁₇ confers on the chromosome which carries it two unique and distinct properties: constitutive function of genes O and P and loss of normal sensitivity to replication inhibition. These properties lead to constitutive replication of λc₁₇ DNA in the immune host and to host killing, even though λc₁₇ does not lyse an immune host and release progeny phage unless it also carries a cI mutation.

A model is presented to explain λc₁₇cI virulence that proposes that those λc₁₇ genes which are subject to cI repression in the immune host can be derepressed if phage replication produces too many phage chromosomes for the cI repressor to control. It is proposed that this derepression can occur only if the replicating element is unable to augment the level of free repressor produced by the prophage, i.e., if it contains a cI mutation.

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Cited by (54)

Isolation and preliminary characterization of Escherichia coli mutants resistant to lethal action of the bacteriophage λ P gene
1991, Virology
Both spontaneous and NTG-induced mutants of Escherichia coli 594 insensitive to the lethal action of λ P gene were isolated and called rpl (resistant to Plethality). These mutants were of two types, showing different phenotypes. On type I rpl mutants, λcl⁻ and λv1 v3 did not plate, while λvir, λcl⁻c17, λimm434, and λimm21 did; plasmid pMR45 carrying the λP gene could not complement λimm21P⁻ phage in type I mutants. On the other hand, the type II rpl mutants support the growth of all the above phages including λcl⁻. Neither type of rpl mutation affects growth of the bacteria.
Genetic analysis of the lytic replicon of bacteriophage P1. I. Isolation and partial characterization
1989, Journal of Molecular Biology
Despite the extensive genetic analysis of bacteriophage P1, the region of the viral genome that is responsible for its lytic (vegetative) replication has not been identified. In this paper we describe the identification of various fragments of P1 DNA that can replicate an otherwise replication-defective λ vector when they are cloned into that vector. The fragments share a 2800 base-pair segment of the P1 genome that is located adjacent to the immI region of the phage. Replication mediated by the cloned P1 fragments is abolished by the product of the P1 cl gene, the repressor of phage lytic functions. Since these properties resemble those of the P1 lytic replicon, we suggest that the 2800 base-pair segment identified here contains that replicon.
hflB, a new Escherichia coli locus regulating lysogeny and the level of bacteriophage lambda cII protein
1986, Journal of Molecular Biology
The level of the viral cII protein has been proposed to be the crucial determinant in the lysis-lysogeny decision of bacteriophage lambda. A new Escherichia coli locus (hflB) has been identified in which a mutation (hflB29) leads to high frequency of lysogeny by λ. A double mutant defective in both hflB and the previously identified hflA gene displays a more severe Hfl⁻ phenotype than either single mutant. The hflB locus is at 69 minutes on the E. coli map, 85% co-transducible with argG. The hflB29 mutation results in increased stability of the phage cII protein (increasing its half-life twofold) and is recessive to hflB⁺. We conclude that the hflB⁺ locus is a negative regulator of cII, perhaps coding for or regulating a protease that acts on cII. In addition, we observe that the can1 mutation, an alteration of the cII gene that results in enhanced lysogenization, leads to increased stability of cII protein. These observations reinforce the view that the level of cII is a key factor in the lysis-lysogeny decision of lambda.
Virulent mutants of bacteriophage φ80
1985, Virology
We have characterized a collection of 11 φ80 mutants that develop in wild-type lysogenic hosts (“virulent” phenotype). All these carry gross DNA rearrangements affecting the right arm of the φ80 chromosome. Our results are consistent with the notion that φ80 development is negatively controlled by the ineA gene product, encoded by one of a cluster of genes (φ80 immunity) located between the φ80 replication and recombination genes. We describe and assign positions for ineA and other genes within the immunity region.
A third defective lambdoid prophage of Escherichia coli K12 defined by the λ derivative, λqin111
1983, Journal of Molecular Biology
We describe the isolation and characterization of a new Q-independent substitution mutant of λ, λqin111, which differs from other characterized Q-independent λ phages. This mutant defines a new λ-like prophage in the bacterial chromosome, as seen by homologous recombination between λqin111 and the host DNA and by DNA/DNA hybridization methods. Genetic and electron microscopy data show that this new prophage carries, at least, genes analogous to Q-S-R of λ and also a cos site functionally identical to λ cos. It is located near 34 min on the Escherichia coli K12 map, i.e. in the same region but at a different site from the defective Rac prophage.
Control of transcription termination: A rho-dependent termination site in bacteriophage lambda
1980, Journal of Molecular Biology
Regulation of gene expression within the bacteriophage λ genome is controlled, in part, by transcriptional termination and anti-termination mechanisms (i.e. attenuation). We define a discrete site, t_R1, in the y region of λ at which transcription termination occurs in vivo. This termination site and the factors which regulate termination at this site in vivo are examined and compared with the previously described in vitro termination reaction. Mutations in the region that enhance (cin-1) or reduce (cnc) termination att_R1 in vitro appear to have similar effects in vivo. The cin-altered t_R1 site appears to be partially resistant to the anti-termination effects of N function. In addition, genetic experiments with cnc mutants suggest the existence of additional termination sites in λ beyond t_R1 but before t_R2.

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Virology

Abstract

References (31)

Repression of the cII and cIII cistrons in a lysogenic bacterium

Virology

Studies in the physiological genetics of some suppressor-sensitive mutants of phage λ

Virology

Sensitive mutants of bacteriophage λ

Virology

Episomes

Advan. Genet.

A membrane-filter technique for the detection of complementary DNA

Biochem. Biophys. Res. Commun.

The action of the λ chromosome. I. The control of functions late in phage development

J. Mol. Biol.

The temperate phage

Genetics and physiology of defective lysogeny in K12 (λ): Studies of early mutants

Virology

The linear insertion of a prophage into the chromosome of E. coli shown by deletion mapping

Biochem. Biophys. Res. Commun.

A quantitative assay for DNA-RNA hybrids with DNA immobilized on a membrane

J. Mol. Biol.

Mutants of bacteriophage λ unable to integrate into the host chromosome

Genetic regulatory mechanisms in the synthesis of proteins

J. Mol. Biol.

Étude génétique d'un bactériophage tempéré d'E. coli. I. Le système génétique du bactériophage λ

Ann. Inst. Pasteur

Sexuality and Genetics of Bacteria

Sur la nature du repressor assurant l'immunité des bactéries lysogènes

Compt. Rend. Acad. Sci.

Cited by (54)

Isolation and preliminary characterization of Escherichia coli mutants resistant to lethal action of the bacteriophage λ P gene

Genetic analysis of the lytic replicon of bacteriophage P1. I. Isolation and partial characterization

hflB, a new Escherichia coli locus regulating lysogeny and the level of bacteriophage lambda cII protein

Virulent mutants of bacteriophage φ80

A third defective lambdoid prophage of Escherichia coli K12 defined by the λ derivative, λqin111

Control of transcription termination: A rho-dependent termination site in bacteriophage lambda