Evidence map›Paper›PMID 23417561›Full record

ArticleEukaryotic cell2013

Factors supporting cysteine tolerance and sulfite production in Candida albicans.

Florian Hennicke, Maria Grumbt, Ulrich Lermann, Nico Ueberschaar, Katja Palige, Bettina Böttcher, Ilse D Jacobsen, Claudia Staib, Joachim Morschhäuser, Michel Monod and 3 more

Open access · diamondAbstract read
In one paragraph

Article in Eukaryotic cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

30 citing papers in PubMed, 51 citations in OpenAlex.

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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

13 authors at 4 institutions in 2 countries.

Florian HennickeLeibniz Institute for Natural Product Research and Infection Biology-Hans Knoell Institute, Junior Research Group Fundamental Molecular Biology of Pathogenic Fungi, Jena, Germany.
Maria Grumbt
Ulrich Lermann
Nico Ueberschaar
Katja Palige
Bettina Böttcher
Ilse D Jacobsen
Claudia Staib
Joachim Morschhäuser
Michel Monod
Bernhard Hube
Christian Hertweck
Peter Staib
Leibniz-Institut für Naturstoff-Forschung und Infektionsbiologie e. V. - Hans-Knöll-Institut (HKI) · DEFriedrich Schiller University Jena · DEUniversity of Würzburg · DEUniversity Hospital of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The amino acid cysteine has long been known to be toxic at elevated levels for bacteria, fungi, and humans. However, mechanisms of cysteine tolerance in microbes remain largely obscure. Here we show that the human pathogenic yeast Candida albicans excretes sulfite when confronted with increasing cysteine concentrations. Mutant construction and phenotypic analysis revealed that sulfite formation from cysteine in C. albicans relies on cysteine dioxygenase Cdg1, an enzyme with similar functions in humans. Environmental cysteine induced not only the expression of the CDG1 gene in C. albicans, but also the expression of SSU1, encoding a putative sulfite efflux pump. Accordingly, the deletion of SSU1 resulted in enhanced sensitivity of the fungal cells to both cysteine and sulfite. To study the regulation of sulfite/cysteine tolerance in more detail, we screened a C. albicans library of transcription factor mutants in the presence of sulfite. This approach and subsequent independent mutant analysis identified the zinc cluster transcription factor Zcf2 to govern sulfite/cysteine tolerance, as well as cysteine-inducible SSU1 and CDG1 gene expression. cdg1Δ and ssu1Δ mutants displayed reduced hypha formation in the presence of cysteine, indicating a possible role of the newly proposed mechanisms of cysteine tolerance and sulfite secretion in the pathogenicity of C. albicans. Moreover, cdg1Δ mutants induced delayed mortality in a mouse model of disseminated infection. Since sulfite is toxic and a potent reducing agent, its production by C. albicans suggests diverse roles during host adaptation and pathogenicity.

Indexed as

AnimalsAnion Transport ProteinsCandida albicansCandidiasisCysteineCysteine DioxygenaseFungal ProteinsGene DeletionGene Expression Regulation, FungalHyphaeMiceMice, Inbred BALB CMutationSulfitesSurvival AnalysisTranscription FactorsAnion Transport ProteinsCysteineCysteine DioxygenaseFungal ProteinsSulfitesTranscription FactorsZinc

Identifiers

PMID23417561
PMCPMC3623443
OpenAlexW2037920917

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.