Evidence map›Paper›PMID 23055925›Full record

ArticlePLoS pathogens2012

DNA mutations mediate microevolution between host-adapted forms of the pathogenic fungus Cryptococcus neoformans.

Denise A Magditch, Tong-Bao Liu, Chaoyang Xue, Alexander Idnurm

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed
4.9field-weighted citation impact, top 5% 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

66 citing papers in PubMed, 86 citations in OpenAlex.

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  14. Similar evolutionary trajectories in an environmentalProceedings of the National Academy of Sciences of the United States of America · 2023
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  15. Article
  16. Review
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  18. Review
  19. Review
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6 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 1 country.

Denise A MagditchDivision of Cell Biology and Biophysics, School of Biological Sciences, University of Missouri-Kansas City, Kansas City, Missouri, United States of America.
Tong-Bao Liu
Chaoyang Xue
Alexander Idnurm
University of Missouri–Kansas City · US

Funding

Light-regulated genes affecting the pathogen potential of Cryptococcus neoformansK22AI073917 · NIAID · UNIVERSITY OF MISSOURI KANSAS CITY · PI IDNURM, ALEXANDER · 2007 to 2008
$268k
NIAID NIH HHS AI073917NIAID NIH HHS K22 AI073917
6 · The paper itself

Abstract

The disease cryptococcosis, caused by the fungus Cryptococcus neoformans, is acquired directly from environmental exposure rather than transmitted person-to-person. One explanation for the pathogenicity of this species is that interactions with environmental predators select for virulence. However, co-incubation of C. neoformans with amoeba can cause a "switch" from the normal yeast morphology to a pseudohyphal form, enabling fungi to survive exposure to amoeba, yet conversely reducing virulence in mammalian models of cryptococcosis. Like other human pathogenic fungi, C. neoformans is capable of microevolutionary changes that influence the biology of the organism and outcome of the host-pathogen interaction. A yeast-pseudohyphal phenotypic switch also happens under in vitro conditions. Here, we demonstrate that this morphological switch, rather than being under epigenetic control, is controlled by DNA mutation since all pseudohyphal strains bear mutations within genes encoding components of the RAM pathway. High rates of isolation of pseudohyphal strains can be explained by the physical size of RAM pathway genes and a hypermutator phenotype of the strain used in phenotypic switching studies. Reversion to wild type yeast morphology in vitro or within a mammalian host can occur through different mechanisms, with one being counter-acting mutations. Infection of mice with RAM mutants reveals several outcomes: clearance of the infection, asymptomatic maintenance of the strains, or reversion to wild type forms and progression of disease. These findings demonstrate a key role of mutation events in microevolution to modulate the ability of a fungal pathogen to cause disease.

Indexed as

Evolution, MolecularGenes, FungalMutationAdaptor Proteins, Signal TransducingAmoebaAnimalsCryptococcosisCryptococcus neoformansDNA, FungalFungal ProteinsHost-Pathogen InteractionsHyphaeMiceMolecular Sequence DataPhenotypeSaccharomyces cerevisiae ProteinsAdaptor Proteins, Signal TransducingDNA, FungalFungal ProteinsSaccharomyces cerevisiae ProteinsTAO3 protein, S cerevisiae

Identifiers

PMID23055925
PMCPMC3464208
OpenAlexW1996882201

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.