Evidence map›Paper›PMID 28793308›Full record

ArticlePLoS genetics2017

Genetic analysis of the Candida albicans biofilm transcription factor network using simple and complex haploinsufficiency.

Virginia E Glazier, Thomas Murante, Daniel Murante, Kristy Koselny, Yuan Liu, Dongyeop Kim, Hyun Koo, Damian J Krysan

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

44 citing papers in PubMed, 56 citations in OpenAlex.

  1. Article
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  14. ThebioRxiv : the preprint server for biology · 2023
    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

8 authors at 2 institutions in 1 country.

Virginia E GlazierDepartment of Pediatrics, University of Rochester Medical Center, Rochester, New York, United States of America.ORCID http://orcid.org/0000-0002-2655-869X
Thomas MuranteDepartment of Pediatrics, University of Rochester Medical Center, Rochester, New York, United States of America.
Daniel MuranteDepartment of Pediatrics, University of Rochester Medical Center, Rochester, New York, United States of America.ORCID http://orcid.org/0000-0001-9909-4702
Kristy KoselnyDepartment of Pediatrics, University of Rochester Medical Center, Rochester, New York, United States of America.
Yuan LiuBiofilm Research Laboratory, Levy Center for Oral Health, Department of Orthodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Dongyeop KimBiofilm Research Laboratory, Levy Center for Oral Health, Department of Orthodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Hyun KooBiofilm Research Laboratory, Levy Center for Oral Health, Department of Orthodontics, School of Dental Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Damian J KrysanDepartment of Pediatrics, University of Rochester Medical Center, Rochester, New York, United States of America.ORCID http://orcid.org/0000-0002-2802-6961
University of Rochester Medical Center · USUniversity of Pennsylvania · US

Funding

S. mutans-C. albicans interactions synergize the virulence of cariogenic biofilmsR01DE025220 · NIDCR · UNIVERSITY OF PENNSYLVANIA · PI KOO, HYUN · 2015 to 2019
$2.0M
Large scale synthetic genetic analysis in Candida albicansR01AI098450 · NIAID · UNIVERSITY OF ROCHESTER · PI KRYSAN, DAMIAN J · 2012 to 2016
$1.9M
NIAID NIH HHS R01 AI098450NIDCR NIH HHS R01 DE025220
6 · The paper itself

Abstract

Biofilm formation by Candida albicans is a key aspect of its pathobiology and is regulated by an integrated network of transcription factors (Bcr1, Brg1, Efg1, Ndt80, Rob1, and Tec1). To understand the details of how the transcription factors function together to regulate biofilm formation, we used a systematic genetic interaction approach based on generating all possible double heterozygous mutants of the network genes and quantitatively analyzing the genetic interactions between them. Overall, the network is highly susceptible to genetic perturbation with the six network heterozygous mutants all showing alterations in biofilm formation (haploinsufficiency). In addition, many double heterozygous mutants are as severely affected as homozygous deletions. As a result, the network shows properties of a highly interdependent 'small-world' network that is highly efficient but not robust. In addition, these genetic interaction data indicate that TEC1 represents a network component whose expression is highly sensitive to small perturbations in the function of other networks TFs. We have also found that expression of ROB1 is dependent on both auto-regulation and cooperative interactions with other network TFs. Finally, the heterozygous NDT80 deletion mutant is hyperfilamentous under both biofilm and hyphae-inducing conditions in a TEC1-dependent manner. Taken together, genetic interaction analysis of this network has provided new insights into the functions of individual TFs as well as into the role of the overall network topology in its function.

Indexed as

BiofilmsGene Expression Regulation, FungalHaploinsufficiencyCandida albicansDNA-Binding ProteinsFungal ProteinsGene DeletionGene Regulatory NetworksTranscription FactorsDNA-Binding ProteinsFungal ProteinsNdt80 protein, Candida albicansTEC1 protein, Candida albicansTranscription Factors

Identifiers

PMID28793308
PMCPMC5565191
OpenAlexW2742366898

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.