Evidence map›Paper›PMID 25504520›Full record

ArticleGenome research2015

Genetic and phenotypic intra-species variation in Candida albicans.

Matthew P Hirakawa, Diego A Martinez, Sharadha Sakthikumar, Matthew Z Anderson, Aaron Berlin, Sharvari Gujja, Qiandong Zeng, Ethan Zisson, Joshua M Wang, Joshua M Greenberg and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Genome research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 239 papers.

0numbers the graph read from it
0cells of the map it votes in
239citing papers in PubMed
–field-weighted citation impact
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

239 citing papers in PubMed, 336 citations in OpenAlex.

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179 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

13 authors at 3 institutions in 2 countries.

Matthew P HirakawaDepartment of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island 02912, USA;
Diego A MartinezBroad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA;
Sharadha SakthikumarBroad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA;
Matthew Z AndersonDepartment of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island 02912, USA; Department of Molecular, Cellular Biology and Genetics, University of Minnesota, Minneapolis, Minnesota 55455, USA;
Aaron BerlinBroad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA;
Sharvari GujjaBroad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA;
Qiandong ZengBroad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA;
Ethan ZissonDepartment of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island 02912, USA;
Joshua M WangDepartment of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island 02912, USA;
Joshua M GreenbergDepartment of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island 02912, USA;
Judith BermanDepartment of Molecular, Cellular Biology and Genetics, University of Minnesota, Minneapolis, Minnesota 55455, USA; Department of Molecular Microbiology and Biotechnology, Tel Aviv University, Ramat Aviv 69978, Israel.
Richard J BennettDepartment of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island 02912, USA; richard_bennett@brown.edu cuomo@broadinstitute.org.
Christina A CuomoBroad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA; richard_bennett@brown.edu cuomo@broadinstitute.org.
Broad Institute · USBrown University · USUniversity of Minnesota · US

Funding

Viral Genomics: evolution, spread, and host interactionsU19AI110818 · NIAID · BROAD INSTITUTE, INC. · PI PARK, DANIEL JOHN · 2014 to 2024
$66.5M
Transcriptional Regulation of C. albicans Cell Fate and Host InteractionsR01AI081704 · NIAID · BROWN UNIVERSITY · PI Richard John Bennett · 2010 to 2026
$6.4M
Centromere Structure and Function in Candida albicansR01AI075096 · NIAID · UNIVERSITY OF MINNESOTA · PI BERMAN, JUDITH G. · 2008 to 2012
$2.6M
Genotypic plasticity and parasex in Candida albicansR21AI112363 · NIAID · BROWN UNIVERSITY · PI BENNETT, RICHARD JOHN · 2014 to 2015
$447k
Parasexual Genetics and Host Adaptation in Candida Fungal PathogensF31DE023726 · NIDCR · BROWN UNIVERSITY · PI HIRAKAWA, MATTHEW · 2014 to 2016
$132k
NIAID NIH HHS AI0624273NIAID NIH HHS AI075096NIAID NIH HHS AI075096-S1NIAID NIH HHS AI081704NIAID NIH HHS AI112363NIAID NIH HHS HHSN272200900018CNIAID NIH HHS R01 AI075096NIAID NIH HHS R01 AI081704NIAID NIH HHS R21 AI112363NIAID NIH HHS U19 AI110818NIDCR NIH HHS F31 DE023726NIDCR NIH HHS F31DE023726PHS HHS HHSN272200900018C
6 · The paper itself

Abstract

Candida albicans is a commensal fungus of the human gastrointestinal tract and a prevalent opportunistic pathogen. To examine diversity within this species, extensive genomic and phenotypic analyses were performed on 21 clinical C. albicans isolates. Genomic variation was evident in the form of polymorphisms, copy number variations, chromosomal inversions, subtelomeric hypervariation, loss of heterozygosity (LOH), and whole or partial chromosome aneuploidies. All 21 strains were diploid, although karyotypic changes were present in eight of the 21 isolates, with multiple strains being trisomic for Chromosome 4 or Chromosome 7. Aneuploid strains exhibited a general fitness defect relative to euploid strains when grown under replete conditions. All strains were also heterozygous, yet multiple, distinct LOH tracts were present in each isolate. Higher overall levels of genome heterozygosity correlated with faster growth rates, consistent with increased overall fitness. Genes with the highest rates of amino acid substitutions included many cell wall proteins, implicating fast evolving changes in cell adhesion and host interactions. One clinical isolate, P94015, presented several striking properties including a novel cellular phenotype, an inability to filament, drug resistance, and decreased virulence. Several of these properties were shown to be due to a homozygous nonsense mutation in the EFG1 gene. Furthermore, loss of EFG1 function resulted in increased fitness of P94015 in a commensal model of infection. Our analysis therefore reveals intra-species genetic and phenotypic differences in C. albicans and delineates a natural mutation that alters the balance between commensalism and pathogenicity.

Indexed as

Genetic VariationPhenotypeAneuploidyCandida albicansCandidiasisChromosomes, FungalDNA Copy Number VariationsEvolution, MolecularGenome, FungalGenotypeHumansPhylogenyPolymorphism, Single NucleotideSelection, GeneticSequence Analysis, DNA

Identifiers

PMID25504520
PMCPMC4352881
OpenAlexW2159359702

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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.