Evidence map›Paper›PMID 9792108›Full record

ArticleProtein science : a publication of the Protein Society1998

Delineation of an evolutionary salvage pathway by compensatory mutations of a defective lysozyme.

M Jucovic, A R Poteete

Open access · bronzeAbstract read
In one paragraph

Article in Protein science : a publication of the Protein Society, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.1field-weighted citation impact, top 57% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed, 6 citations in OpenAlex.

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4 · The record

Corrections and comments

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5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

M JucovicDepartment of Molecular Genetics and Microbiology, University of Massachusetts Medical Center, Worcester 01655, USA.
A R Poteete
University of Massachusetts Chan Medical School · US

Funding

GENETIC ANALYSIS OF BACTERIOPHAGE LYSOZYME STRUCTURER01AI024083 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI POTEETE, ANTHONY R. · 1988 to 1997
–
NIAID NIH HHS AI24083
6 · The paper itself

Abstract

Model-free approaches (random mutagenesis, DNA shuffling) in combination with more "rational," three-dimensional information-guided randomization have been used for directed evolution of lysozyme activity in a defective T4 lysozyme mutant. A specialized lysozyme cloning vector phage, derived from phage lambda, depends upon T4 lysozyme function for its ability to form plaques. The substitution W138P in T4 lysozyme totally abolishes its plaque-forming ability. Compensating mutations in W138P T4 lysozyme after sequential random mutagenesis of the whole gene as well as after targeted randomization of residues in the vicinity of Trp138 were selected. In a second stage, these mutations were randomly recombined by the recombinatorial PCR method of DNA shuffling. Shuffled and selected W138P T4 lysozyme variants provide the hybrid lambda phage with sufficient lysozyme activity to produce normal-size plaques, even at elevated temperature (42 degrees C). The individual mutations with the highest compensatory information for W138P repair are the substitutions A146F and A146M, selected after targeted randomization of three residues in the neighborhood of Trp138 by combinatorial mutagenesis. The best evolved W138P T4 lysozymes, however, accumulated mutations originating from both randomly mutagenized as well as target-randomized variants.

Indexed as

Evolution, MolecularBacteriophage lambdaBacteriophage T4CodonDNA, ViralGenetic VectorsModels, MolecularMuramidaseMutagenesisMutationPolymerase Chain ReactionRecombination, GeneticSuppression, GeneticCodonDNA, ViralMuramidase

Identifiers

PMID9792108
PMCPMC2143835
OpenAlexW1975248115

What OpenQuestion holds

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.