Evidence map›Paper›PMID 25409341›Full record

ArticlePloS one2014

Frequency and fitness consequences of bacteriophage φ6 host range mutations.

Brian E Ford, Bruce Sun, James Carpino, Elizabeth S Chapler, Jane Ching, Yoon Choi, Kevin Jhun, Jung D Kim, Gregory G Lallos, Rachelle Morgenstern and 3 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

22 citing papers in PubMed, 41 citations in OpenAlex.

  1. Review
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  5. Bioinformatics advances · 2025
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  20. Evolutionary ecology of virus emergence.Annals of the New York Academy of Sciences · 2017
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 1 institution in 1 country.

Brian E FordBiology Department, Queens College of the City University of New York, New York, New York, United States of America; The Graduate Center of the City University of New York, New York, New York, United States of America.
Bruce SunBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
James CarpinoBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
Elizabeth S ChaplerBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
Jane ChingBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
Yoon ChoiBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
Kevin JhunBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
Jung D KimBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
Gregory G LallosBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
Rachelle MorgensternBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
Shalini SinghBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
Sai ThejaBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
John J DennehyBiology Department, Queens College of the City University of New York, New York, New York, United States of America.
Queens College, CUNY · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Viruses readily mutate and gain the ability to infect novel hosts, but few data are available regarding the number of possible host range-expanding mutations allowing infection of any given novel host, and the fitness consequences of these mutations on original and novel hosts. To gain insight into the process of host range expansion, we isolated and sequenced 69 independent mutants of the dsRNA bacteriophage Φ6 able to infect the novel host, Pseudomonas pseudoalcaligenes. In total, we found at least 17 unique suites of mutations among these 69 mutants. We assayed fitness for 13 of 17 mutant genotypes on P. pseudoalcaligenes and the standard laboratory host, P. phaseolicola. Mutants exhibited significantly lower fitnesses on P. pseudoalcaligenes compared to P. phaseolicola. Furthermore, 12 of the 13 assayed mutants showed reduced fitness on P. phaseolicola compared to wildtype Φ6, confirming the prevalence of antagonistic pleiotropy during host range expansion. Further experiments revealed that the mechanistic basis of these fitness differences was likely variation in host attachment ability. In addition, using computational protein modeling, we show that host-range expanding mutations occurred in hotspots on the surface of the phage's host attachment protein opposite a putative hydrophobic anchoring domain.

Indexed as

Bacteriophage phi 6Binding SitesGenetic FitnessHost SpecificityModels, MolecularMutation RatePseudomonas pseudoalcaligenesSequence Analysis, RNAViral ProteinsViral Proteins

Identifiers

PMID25409341
PMCPMC4237377
OpenAlexW2166143292

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.