Evidence map›Paper›PMID 24353214›Full record

ReviewThe Journal of experimental biology2014

Stress adaptation in a pathogenic fungus.

Alistair J P Brown, Susan Budge, Despoina Kaloriti, Anna Tillmann, Mette D Jacobsen, Zhikang Yin, Iuliana V Ene, Iryna Bohovych, Doblin Sandai, Stavroula Kastora and 5 more

Abstract readReview
In one paragraph

Review in The Journal of experimental biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers.

0numbers the graph read from it
0cells of the map it votes in
172citing 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

172 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
  5. Article
  6. Morphotype-specific susceptibility toMicrobiology spectrum · 2026
    Article
  7. Paralogs of thebioRxiv : the preprint server for biology · 2026
    Article
  8. Article
  9. Insights on molecular drivers of phenotypic plasticity in Candidozyma auris.World journal of microbiology & biotechnology · 2026
    Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Stress-responsive roles of thebioRxiv : the preprint server for biology · 2026
    Article
  17. Article
  18. Article
  19. Trainable computation in molecular networks.bioRxiv : the preprint server for biology · 2025
    Article
  20. DVL, a Lectin fromAntibiotics (Basel, Switzerland) · 2025
    Article

112 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

15 authors.

Alistair J P BrownSchool of Medical Sciences, University of Aberdeen, Institute of Medical Sciences, Foresterhill, Aberdeen AB25 2ZD, UK.
Susan Budge
Despoina Kaloriti
Anna Tillmann
Mette D Jacobsen
Zhikang Yin
Iuliana V Ene
Iryna Bohovych
Doblin Sandai
Stavroula Kastora
Joanna Potrykus
Elizabeth R Ballou
Delma S Childers
Shahida Shahana
Michelle D Leach

Funding

Biotechnology and Biological Sciences Research Council BB/C510391/1Biotechnology and Biological Sciences Research Council BB/D009308/1Biotechnology and Biological Sciences Research Council BB/F000111/1Biotechnology and Biological Sciences Research Council BB/F00513X/1Biotechnology and Biological Sciences Research Council BB/F010826/1Biotechnology and Biological Sciences Research Council BBS/B/06679Wellcome TrustWellcome Trust 080088Wellcome Trust 096072Wellcome Trust 097377
6 · The paper itself

Abstract

Candida albicans is a major fungal pathogen of humans. This yeast is carried by many individuals as a harmless commensal, but when immune defences are perturbed it causes mucosal infections (thrush). Additionally, when the immune system becomes severely compromised, C. albicans often causes life-threatening systemic infections. A battery of virulence factors and fitness attributes promote the pathogenicity of C. albicans. Fitness attributes include robust responses to local environmental stresses, the inactivation of which attenuates virulence. Stress signalling pathways in C. albicans include evolutionarily conserved modules. However, there has been rewiring of some stress regulatory circuitry such that the roles of a number of regulators in C. albicans have diverged relative to the benign model yeasts Saccharomyces cerevisiae and Schizosaccharomyces pombe. This reflects the specific evolution of C. albicans as an opportunistic pathogen obligately associated with warm-blooded animals, compared with other yeasts that are found across diverse environmental niches. Our understanding of C. albicans stress signalling is based primarily on the in vitro responses of glucose-grown cells to individual stresses. However, in vivo this pathogen occupies complex and dynamic host niches characterised by alternative carbon sources and simultaneous exposure to combinations of stresses (rather than individual stresses). It has become apparent that changes in carbon source strongly influence stress resistance, and that some combinatorial stresses exert non-additive effects upon C. albicans. These effects, which are relevant to fungus-host interactions during disease progression, are mediated by multiple mechanisms that include signalling and chemical crosstalk, stress pathway interference and a biological transistor.

Indexed as

Adaptation, PhysiologicalCandida albicansFungal ProteinsGlucoseHeat-Shock ResponseMitogen-Activated Protein KinasesOsmotic PressureOxidative StressSaccharomyces cerevisiaeSchizosaccharomycesSignal TransductionFungal ProteinsGlucoseMitogen-Activated Protein KinasesCandida albicansCarbon metabolismCationic stressFungal pathogenicityHeat shockNitrosative stressOsmotic stressOxidative stressStress adaptation

Identifiers

PMID24353214
PMCPMC3867497

What OpenQuestion holds

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LicenceCC BY-NC-SA
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.