Evidence map›Paper›PMID 24034898›Full record

ArticleBMC genomics2013

Comparative genomics of emerging pathogens in the Candida glabrata clade.

Toni Gabaldón, Tiphaine Martin, Marina Marcet-Houben, Pascal Durrens, Monique Bolotin-Fukuhara, Olivier Lespinet, Sylvie Arnaise, Stéphanie Boisnard, Gabriela Aguileta, Ralitsa Atanasova and 20 more

Abstract read
In one paragraph

Article in BMC genomics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 123 papers.

0numbers the graph read from it
0cells of the map it votes in
123citing 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

123 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Journal of medical microbiology · 2026
    Review
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  7. Journal of medical microbiology · 2026
    Review
  8. Article
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  10. Genetic and environmental control of parasexual reproduction in the pathogenicMicrobiology and molecular biology reviews : MMBR · 2025
    Review
  11. An update on clinically relevant, rare, and emergingClinical microbiology reviews · 2025
    Review
  12. Article
  13. Article
  14. Heterogeneity ofMicrobiology spectrum · 2025
    Article
  15. Article
  16. mSphere · 2024
    Article
  17. Article
  18. Article
  19. Article
  20. The Enigma ofMicroorganisms · 2024
    Article

63 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

30 authors.

Toni GabaldónBioinformatics and Genomics Programme, Centre for Genomic Regulation (CRG) and UPF, Doctor Aiguader, 88, Barcelona, 08003, Spain. toni.gabaldon@crg.eu.
Tiphaine Martin
Marina Marcet-Houben
Pascal Durrens
Monique Bolotin-Fukuhara
Olivier Lespinet
Sylvie Arnaise
Stéphanie Boisnard
Gabriela Aguileta
Ralitsa Atanasova
Christiane Bouchier
Arnaud Couloux
Sophie Creno
Jose Almeida Cruz
Hugo Devillers
Adela Enache-Angoulvant
Juliette Guitard
Laure Jaouen
Laurence Ma
Christian Marck
Cécile Neuvéglise
Eric Pelletier
Amélie Pinard
Julie Poulain
Julien Recoquillay
Eric Westhof
Patrick Wincker
Bernard Dujon
Christophe Hennequin
Cécile Fairhead

Funding

European Research Council 310325
6 · The paper itself

Abstract

backgroundCandida glabrata follows C. albicans as the second or third most prevalent cause of candidemia worldwide. These two pathogenic yeasts are distantly related, C. glabrata being part of the Nakaseomyces, a group more closely related to Saccharomyces cerevisiae. Although C. glabrata was thought to be the only pathogenic Nakaseomyces, two new pathogens have recently been described within this group: C. nivariensis and C. bracarensis. To gain insight into the genomic changes underlying the emergence of virulence, we sequenced the genomes of these two, and three other non-pathogenic Nakaseomyces, and compared them to other sequenced yeasts.

resultsOur results indicate that the two new pathogens are more closely related to the non-pathogenic N. delphensis than to C. glabrata. We uncover duplications and accelerated evolution that specifically affected genes in the lineage preceding the group containing N. delphensis and the three pathogens, which may provide clues to the higher propensity of this group to infect humans. Finally, the number of Epa-like adhesins is specifically enriched in the pathogens, particularly in C. glabrata.

conclusionsRemarkably, some features thought to be the result of adaptation of C. glabrata to a pathogenic lifestyle, are present throughout the Nakaseomyces, indicating these are rather ancient adaptations to other environments. Phylogeny suggests that human pathogenesis evolved several times, independently within the clade. The expansion of the EPA gene family in pathogens establishes an evolutionary link between adhesion and virulence phenotypes. Our analyses thus shed light onto the relationships between virulence and the recent genomic changes that occurred within the Nakaseomyces. SEQUENCE ACCESSION NUMBERS: Nakaseomyces delphensis: CAPT01000001 to CAPT01000179Candida bracarensis: CAPU01000001 to CAPU01000251Candida nivariensis: CAPV01000001 to CAPV01000123Candida castellii: CAPW01000001 to CAPW01000101Nakaseomyces bacillisporus: CAPX01000001 to CAPX01000186.

Indexed as

Genome, FungalPhylogenyCandida glabrataDNA, FungalEvolution, MolecularSaccharomycetalesSelection, GeneticSequence Analysis, DNADNA, Fungal

Identifiers

PMID24034898
PMCPMC3847288

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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.