Evidence map›Paper›PMID 33989396›Full record

ArticleGenetics2021

Environmentally contingent control of Candida albicans cell wall integrity by transcriptional regulator Cup9.

Yuichi Ichikawa, Vincent M Bruno, Carol A Woolford, Hannah Kim, Eunsoo Do, Grace C Brewer, Aaron P Mitchell

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.3field-weighted citation impact, top 43% 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

6 citing papers in PubMed, 7 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

7 authors at 4 institutions in 2 countries.

Yuichi IchikawaDepartment of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA 15213, USA.
Vincent M BrunoDepartment of Microbiology and Immunology and Institute of Genome Sciences, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
Carol A WoolfordDepartment of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA 15213, USA.
Hannah KimDepartment of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA 15213, USA.ORCID 0000-0002-6366-1741
Eunsoo DoDepartment of Microbiology, University of Georgia, Athens, GA 30602, USA.
Grace C BrewerDepartment of Microbiology, University of Georgia, Athens, GA 30602, USA.
Aaron P MitchellDepartment of Biological Sciences, Carnegie Mellon University, Pittsburgh, PA 15213, USA.ORCID 0000-0002-0868-4000
University of Georgia · USCarnegie Mellon University · USThe Cancer Institute Hospital · JPUniversity of Maryland, Baltimore · US

Funding

C. ALBICANS HYPHAL CELL WALL STRESS RESPONSER21AI137464 · NIAID · CARNEGIE-MELLON UNIVERSITY · PI MITCHELL, AARON P · 2018 to 2019
$414k
NIAID NIH HHS R21 AI137464
6 · The paper itself

Abstract

The fungal pathogen Candida albicans is surrounded by a cell wall that is the target of caspofungin and other echinocandin antifungals. Candida albicans can grow in several morphological forms, notably budding yeast and hyphae. Yeast and hyphal forms differ in cell wall composition, leading us to hypothesize that there may be distinct genes required for yeast and hyphal responses to caspofungin. Mutants in 27 genes reported previously to be caspofungin hypersensitive under yeast growth conditions were all caspofungin hypersensitive under hyphal growth conditions as well. However, a screen of mutants defective in transcription factor genes revealed that Cup9 is required for normal caspofungin tolerance under hyphal and not yeast growth conditions. In a hyphal-defective efg1Δ/Δ background, Cup9 is still required for normal caspofungin tolerance. This result argues that Cup9 function is related to growth conditions rather than cell morphology. RNA-seq conducted under hyphal growth conditions indicated that 361 genes were up-regulated and 145 genes were down-regulated in response to caspofungin treatment. Both classes of caspofungin-responsive genes were enriched for cell wall-related proteins, as expected for a response to disruption of cell wall integrity and biosynthesis. The cup9Δ/Δ mutant, treated with caspofungin, had reduced RNA levels of 40 caspofungin up-regulated genes, and had increased RNA levels of 8 caspofungin down-regulated genes, an indication that Cup9 has a narrow rather than global role in the cell wall integrity response. Five Cup9-activated surface-protein genes have roles in cell wall integrity, based on mutant analysis published previously (PGA31 and IFF11) or shown here (ORF19.3499, ORF19.851, or PGA28), and therefore may explain the hypersensitivity of the cup9Δ/Δmutant to caspofungin. Our findings define Cup9 as a new determinant of caspofungin susceptibility.

Indexed as

Drug Resistance, FungalAntifungal AgentsCandida albicansCaspofunginCell WallFungal ProteinsGene Expression Regulation, FungalHomeodomain ProteinsTranscription FactorsAntifungal AgentsCaspofunginFungal ProteinsHomeodomain ProteinsTranscription FactorsCandidacell wall integrityregulation

Identifiers

PMID33989396
PMCPMC8864738
OpenAlexW3160048571

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.