Evidence map›Paper›PMID 22544909›Full record

ArticleEukaryotic cell2012

Divergent targets of Candida albicans biofilm regulator Bcr1 in vitro and in vivo.

Saranna Fanning, Wenjie Xu, Norma Solis, Carol A Woolford, Scott G Filler, Aaron P Mitchell

Open access · diamondAbstract read
In one paragraph

Article in Eukaryotic cell, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.

0numbers the graph read from it
0cells of the map it votes in
78citing papers in PubMed
5.8field-weighted citation impact, top 3% 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

78 citing papers in PubMed, 112 citations in OpenAlex.

  1. Article
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  9. Microorganisms · 2025
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  14. The role of theCell surface (Amsterdam, Netherlands) · 2023
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  16. bioRxiv : the preprint server for biology · 2023
    Article
  17. UsingVirulence · 2022
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  19. Frontiers in immunology · 2022
    Article
  20. Article

18 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

6 authors at 2 institutions in 1 country.

Saranna FanningDepartment of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania, USA.
Wenjie Xu
Norma Solis
Carol A Woolford
Scott G Filler
Aaron P Mitchell
Carnegie Mellon University · USThe Lundquist Institute · US

Funding

Candida albicans Epithelial Cell Interactions and Oropharyngeal DiseaseR01DE017088 · NIDCR · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI FILLER, SCOTT G · 2005 to 2014
$3.4M
GENETIC CONTROL OF C. ALBICANS BIOFILM FORMATIONR01AI067703 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MITCHELL, AARON P · 2006 to 2014
$3.2M
PATHOGENESIS OF OROPHARYNGEAL CANDIDIASISR01DE013974 · NIDCR · LA BIOMED RES INST/ HARBOR UCLA MED CTR · PI FILLER, SCOTT G · 2000 to 2004
$1.4M
NIAID NIH HHS R01 AI067703NIDCR NIH HHS R01 DE013974NIDCR NIH HHS R01 DE017088
6 · The paper itself

Abstract

Candida albicans is a causative agent of oropharyngeal candidiasis (OPC), a biofilm-like infection of the oral mucosa. Biofilm formation depends upon the C. albicans transcription factor Bcr1, and previous studies indicate that Bcr1 is required for OPC in a mouse model of infection. Here we have used a nanoString gene expression measurement platform to elucidate the role of Bcr1 in OPC-related gene expression. We chose for assays a panel of 134 genes that represent a range of morphogenetic and cell cycle functions as well as environmental and stress response pathways. We assayed gene expression in whole infected tongue samples. The results sketch a portrait of C. albicans gene expression in which numerous stress response pathways are activated during OPC. This one set of experiments identifies 64 new genes with significantly altered RNA levels during OPC, thus increasing substantially the number of known genes in this expression class. The bcr1Δ/Δ mutant had a much more limited gene expression defect during OPC infection than previously reported for in vitro growth conditions. Among major functional Bcr1 targets, we observed that ALS3 was Bcr1 dependent in vivo while HWP1 was not. We used null mutants and complemented strains to verify that Bcr1 and Hwp1 are required for OPC infection in this model. The role of Als3 is transient and mild, though significant. Our findings suggest that the versatility of C. albicans as a pathogen may reflect its ability to persist in the face of multiple stresses and underscore that transcriptional circuitry during infection may be distinct from that detailed during in vitro growth.

Indexed as

BiofilmsGene Expression Regulation, FungalAnimalsCandida albicansCandidiasis, OralDisease Models, AnimalFungal ProteinsHumansMaleMiceMice, Inbred BALB CMouth MucosaFungal Proteins

Identifiers

PMID22544909
PMCPMC3416506
OpenAlexW2136685344

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.