Evidence map›Paper›PMID 26297702›Full record

ArticleEukaryotic cell2015

MIG1 Regulates Resistance of Candida albicans against the Fungistatic Effect of Weak Organic Acids.

Fabien Cottier, Alrina Shin Min Tan, Xiaoli Xu, Yue Wang, Norman Pavelka

Open access · diamondAbstract read
In one paragraph

Article in Eukaryotic cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

18 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  7. Human PathogenicJournal of fungi (Basel, Switzerland) · 2020
    Article
  8. Review
  9. Review
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  13. The mammalian mycobiome: A complex system in a dynamic relationship with the host.Wiley interdisciplinary reviews. Systems biology and medicine · 2019
    Review
  14. Article
  15. The Transcriptional Response ofG3 (Bethesda, Md.) · 2017
    Article
  16. 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

5 authors at 1 institution in 1 country.

Fabien CottierSingapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Alrina Shin Min TanSingapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Xiaoli XuInstitute of Molecular and Cell Biology, A*STAR, Singapore, Singapore.
Yue WangInstitute of Molecular and Cell Biology, A*STAR, Singapore, Singapore.
Norman PavelkaSingapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore norman_pavelka@immunol.a-star.edu.sg.ORCID http://orcid.org/0000-0003-4542-9970
Agency for Science, Technology and Research · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Candida albicans is the leading cause of fungal infections; but it is also a member of the human microbiome, an ecosystem of thousands of microbial species potentially influencing the outcome of host-fungal interactions. Accordingly, antibacterial therapy raises the risk of candidiasis, yet the underlying mechanism is currently not fully understood. We hypothesize the existence of bacterial metabolites that normally control C. albicans growth and of fungal resistance mechanisms against these metabolites. Among the most abundant microbiota-derived metabolites found on human mucosal surfaces are weak organic acids (WOAs), such as acetic, propionic, butyric, and lactic acid. Here, we used quantitative growth assays to investigate the dose-dependent fungistatic properties of WOAs on C. albicans growth and found inhibition of growth to occur at physiologically relevant concentrations and pH values. This effect was conserved across distantly related fungal species both inside and outside the CTG clade. We next screened a library of transcription factor mutants and identified several genes required for the resistance of C. albicans to one or more WOAs. A single gene, MIG1, previously known for its role in glucose repression, conferred resistance against all four acids tested. Consistent with glucose being an upstream activator of Mig1p, the presence of this carbon source was required for WOA resistance in wild-type C. albicans. Conversely, a MIG1-complemented strain completely restored the glucose-dependent resistance against WOAs. We conclude that Mig1p plays a central role in orchestrating a transcriptional program to fight against the fungistatic effect of this class of highly abundant metabolites produced by the gastrointestinal tract microbiota.

Indexed as

Acetic AcidAntifungal AgentsButyric AcidCandida albicansCandidiasisDrug Resistance, FungalFungal ProteinsLactic AcidMicrobial Sensitivity TestsPropionatesRepressor ProteinsAcetic AcidAntifungal AgentsButyric AcidFungal ProteinsLactic AcidPropionatespropionic acidRepressor Proteins

Identifiers

PMID26297702
PMCPMC4588629
OpenAlexW2171806420

What OpenQuestion holds

Textmetadata
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.