Mutations that detoxify an aberrant T4 membrane protein

Nelson, Mary Anne; Singer, Britta Swebilius; Gold, Larry; Pribnow, David

doi:10.1016/0022-2836(81)90478-2

Cited by 19 publications

(8 citation statements)

References 32 publications

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“…This mechanism serves to extend and to perfect the homology between imperfect direct repeat sequences. This class of mutations, called ‘dislocation’ or ‘quasi‐repeat’ mutations, were proposed to explain certain mutational hot‐spots (Fowler et al ., 1974; Nelson et al ., 1981) and later observed in mutational spectra derived from in vitro polymerization by enzymes from eukaryotic sources (Kunkel and Soni, 1988; Kunkel, 1990). Dislocation mutations have been deduced from features of mutational spectra from E. coli in vivo (Fowler et al ., 1986; Schaaper et al ., 1986; Schaaper, 1988) .…”

Section: Transient Misalignment Between Short Direct Repeats: ‘Dislocmentioning

confidence: 99%

Encoded errors: mutations and rearrangements mediated by misalignment at repetitive DNA sequences

Lovett

2004

Molecular Microbiology

242

215

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SummaryMutations and rearrangements that occur by misalignment during DNA replication are frequent sources of genetic variation in bacteria. Dislocations between a replicating strand and its template at repetitive DNA sequences underlie the mechanism of these genetic events. Such misalignments can be transient or stable and can involve intramolecular or intermolecular DNA mispairing, even pairing across a replication fork. Paradoxically, these replication 'slippage' events both create and destroy repetitive sequences in bacterial genomes. This review catalogues several types of slippage errors, presents the cellular processes that act to limit them and discusses the consequences of this class of genetic events on the evolution of bacterial genomes and physiology.

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Section: Transient Misalignment Between Short Direct Repeats: ‘Dislocmentioning

confidence: 99%

Encoded errors: mutations and rearrangements mediated by misalignment at repetitive DNA sequences

Lovett

2004

Molecular Microbiology

242

215

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“…LG90(prex20) cultures were grown in the presence of 25 ,ug of chloramphenicol per ml. "Average number of progeny phage yielded per infected bacterium.…”

Section: Resultsmentioning

confidence: 99%

“…The rII and possibly the rexA proteins are found in the membrane (19,29,42), and there is some evidence that the rex proteins may be involved in cell lysis (4). Two rll phenomena independent of rex are the rapid lysis phenotype (12) and the toxic effect of the rlIB polypeptide encoded by mutants FC237 and FC238 (25). These are both cell lysis phenomena and presumably involve the membrane.…”

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confidence: 99%

Wild-type bacteriophage T4 is restricted by the lambda rex genes

Shinedling

Parma

Gold

1987

J Virol

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The bacteriophage T4 rII genes and the lambda rex (r exclusion) genes interact; rll mutants are unable to productively infect rex+ lambda lysogens. The relationship between rex and rll has been found to be quantitative, and plasmid clones of rex have excluded not only rII mutants but T4 wild type and most other bacteriophages as well. Mutations in the T4 motA gene substantially reversed exclusion of T4 by rex.

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“…One possibility is a sampling anomaly. Another is that the deletions but not the additions result in a toxic polypeptide, a phenomenon already encountered with a frameshift mutation in the rIIB gene (31). Yet another possibility is translation reinitiation (30), wherein the Ϫ1 reading frame creates a UAG termination codon at new codon 10, which is followed about 9 codons farther along by an AUG codon in the normal rIV reading frame that might suffice to reinitiate a functional protein.…”

Section: Vol 193 2011mentioning

confidence: 99%

The Bacteriophage T4 Rapid-Lysis Genes and Their Mutational Proclivities

Burch¹,

Zhang²,

Chao³

et al. 2011

Journal of Bacteriology

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Like most phages with double-stranded DNA, phage T4 exits the infected host cell by a lytic process requiring, at a minimum, an endolysin and a holin. Unlike most phages, T4 can sense superinfection (which signals the depletion of uninfected host cells) and responds by delaying lysis and achieving an order-ofmagnitude increase in burst size using a mechanism called lysis inhibition (LIN). T4 r mutants, which are unable to conduct LIN, produce distinctly large, sharp-edged plaques. The discovery of r mutants was key to the foundations of molecular biology, in particular to discovering and characterizing genetic recombination in T4, to redefining the nature of the gene, and to exploring the mutation process at the nucleotide level of resolution. A number of r genes have been described in the past 7 decades with various degrees of clarity. Here we describe an extensive and perhaps saturating search for T4 r genes and relate the corresponding mutational spectra to the often imperfectly known physiologies of the proteins encoded by these genes. Focusing on r genes whose mutant phenotypes are largely independent of the host cell, the genes are rI (which seems to sense superinfection and signal the holin to delay lysis), rIII (of poorly defined function), rIV (same as sp and also of poorly defined function), and rV (same as t, the holin gene). We did not identify any mutations that might correspond to a putative rVI gene, and we did not focus on the famous rII genes because they appear to affect lysis only indirectly.The classical T-even phages T2, T4, and T6 infect many strains of Escherichia coli and related genera and produce plaques with fuzzy edges. Occasional mutants produce larger plaques with sharp edges. When liquid cultures of exponentially growing host cells are infected with the wild-type phage, lysis occurs only after several hours and results in titers that can exceed 10 11 virions/ml. However, when such cultures are infected with the large-plaque mutants, they typically clear much more rapidly and display titers on the order of 10 9 virions/ml. These mutants were accordingly named "r" for rapid lysis (20) and reflect the failure of the process of lysis inhibition (LIN), wherein cells that are reinfected ("superinfected") several minutes after the first infection greatly extend their latent periods and produce much larger burst sizes (12). This is a highly effective mechanism that senses the impending local disappearance of uninfected host cells and adopts a strategy that maximizes the final yield of progeny. As such, it has long been of interest not only to virologists but also to students of evolution and life histories.Genetic studies in the 1940s to 1960s, mainly using T2 and T4, defined three r loci, rI, rII, and rIII, while subsequent studies implicated three more loci, rIV, rV, and rVI. Based mainly on summarized T4 genomics (28), map locations of confirmed r genes (rI to rV) and related genes are shown in Fig. 1 and some parameters of genes rI through rV are summarized in Table 1. We sought to de...

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Mutations that detoxify an aberrant T4 membrane protein

Cited by 19 publications

References 32 publications

Encoded errors: mutations and rearrangements mediated by misalignment at repetitive DNA sequences

Encoded errors: mutations and rearrangements mediated by misalignment at repetitive DNA sequences

Wild-type bacteriophage T4 is restricted by the lambda rex genes

The Bacteriophage T4 Rapid-Lysis Genes and Their Mutational Proclivities

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