Evidence map›Paper›PMID 31091232›Full record

ArticlePLoS genetics2019

Selection of Candida albicans trisomy during oropharyngeal infection results in a commensal-like phenotype.

Anja Forche, Norma V Solis, Marc Swidergall, Robert Thomas, Alison Guyer, Annette Beach, Gareth A Cromie, Giang T Le, Emily Lowell, Norman Pavelka and 4 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
5.1field-weighted citation impact, top 4% 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

41 citing papers in PubMed, 56 citations in OpenAlex.

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  13. Microbiology and molecular biology reviews : MMBR · 2024
    Review
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  15. Article
  16. Aneuploidy and gene dosage regulate filamentation and host colonization byProceedings of the National Academy of Sciences of the United States of America · 2023
    Article
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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

14 authors at 7 institutions in 3 countries.

Anja ForcheDepartment of Biology, Bowdoin College, Brunswick, Maine, United States of America.ORCID 0000-0002-3004-5176
Norma V SolisDivision of Infectious Diseases, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, United States of America.
Marc SwidergallDivision of Infectious Diseases, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, United States of America.ORCID 0000-0002-5261-6267
Robert ThomasDepartment of Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, Nebraska, United States of America.
Alison GuyerDepartment of Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, Nebraska, United States of America.
Annette BeachDepartment of Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, Nebraska, United States of America.
Gareth A CromiePacific Northwest Research Institute, Seattle, Washington, United States of America.ORCID 0000-0001-5265-1970
Giang T LeSingapore Immunology Network (SIgN), Agency of Science, Technology and Research (A*STAR), Singapore, Singapore.
Emily LowellDepartment of Biology, Bowdoin College, Brunswick, Maine, United States of America.
Norman PavelkaSingapore Immunology Network (SIgN), Agency of Science, Technology and Research (A*STAR), Singapore, Singapore.
Judith BermanSchool of Molecular Cell Biology and Biotechnology, Tel Aviv University, Tel Aviv, Israel.ORCID 0000-0002-8577-0084
Aimeé M DudleyPacific Northwest Research Institute, Seattle, Washington, United States of America.ORCID 0000-0003-3644-0625
Anna SelmeckiDepartment of Medical Microbiology and Immunology, Creighton University School of Medicine, Omaha, Nebraska, United States of America.
Scott G FillerDivision of Infectious Diseases, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, Torrance, California, United States of America.ORCID 0000-0001-7278-3700
Creighton University · USAgency for Science, Technology and Research · SGBowdoin College · USPacific Northwest Diabetes Research Institute · USThe Lundquist Institute · USTel Aviv University · ILUniversity of California, Los Angeles · US

Funding

TRANSGENIC EXPRESSION ANALYSIS OF MIRNA-144P20RR018788 · NCRR · UNIVERSITY OF NEBRASKA MEDICAL CENTER · PI WESTON, MICHAEL D · 2003 to 2011
$16.5M
Endothelial invasion by yeast-phase CandidaR01AI124566 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI FILLER, SCOTT G, MITCHELL, AARON P · 2016 to 2020
$2.7M
Role of genome plasticity in Candida albicans host-pathogen interactionsR15AI090633 · NIAID · BOWDOIN COLLEGE · PI FORCHE, ANJA · 2011 to 2018
$1.1M
Novel Candida albicans host receptors during infection and immune responseK99DE026856 · NIDCR · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI SWIDERGALL, MARC · 2017 to 2018
$267k
NCRR NIH HHS P20 RR018788NIAID NIH HHS R01 AI124566NIAID NIH HHS R15 AI090633NIDCR NIH HHS K99 DE026856
6 · The paper itself

Abstract

When the fungus Candida albicans proliferates in the oropharyngeal cavity during experimental oropharyngeal candidiasis (OPC), it undergoes large-scale genome changes at a much higher frequency than when it grows in vitro. Previously, we identified a specific whole chromosome amplification, trisomy of Chr6 (Chr6x3), that was highly overrepresented among strains recovered from the tongues of mice with OPC. To determine the functional significance of this trisomy, we assessed the virulence of two Chr6 trisomic strains and a Chr5 trisomic strain in the mouse model of OPC. We also analyzed the expression of virulence-associated traits in vitro. All three trisomic strains exhibited characteristics of a commensal during OPC in mice. They achieved the same oral fungal burden as the diploid progenitor strain but caused significantly less weight loss and elicited a significantly lower inflammatory host response. In vitro, all three trisomic strains had reduced capacity to adhere to and invade oral epithelial cells and increased susceptibility to neutrophil killing. Whole genome sequencing of pre- and post-infection isolates found that the trisomies were usually maintained. Most post-infection isolates also contained de novo point mutations, but these were not conserved. While in vitro growth assays did not reveal phenotypes specific to de novo point mutations, they did reveal novel phenotypes specific to each lineage. These data reveal that during OPC, clones that are trisomic for Chr5 or Chr6 are selected and they facilitate a commensal-like phenotype.

Indexed as

AnimalsCandida albicansCandidiasisCandidiasis, OralDisease Models, AnimalEpithelial CellsMaleMiceMice, Inbred BALB CNeutrophilsOropharynxPhenotypeTrisomyVirulence

Identifiers

PMID31091232
PMCPMC6538192
OpenAlexW2914202307

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.