Evidence map›Paper›PMID 16552442›Full record

ArticlePLoS pathogens2006

Control of the C. albicans cell wall damage response by transcriptional regulator Cas5.

Vincent M Bruno, Sergey Kalachikov, Ryan Subaran, Clarissa J Nobile, Christos Kyratsous, Aaron P Mitchell

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers.

0numbers the graph read from it
0cells of the map it votes in
103citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

103 citing papers in PubMed, 161 citations in OpenAlex.

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  8. Journal of fungi (Basel, Switzerland) · 2024
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  13. The Role of Sfp1 inJournal of fungi (Basel, Switzerland) · 2022
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  14. Caspofungin resistance in Candida albicans: genetic factors and synergistic compounds for combination therapies.Brazilian journal of microbiology : [publication of the Brazilian Society for Microbiology] · 2022
    Review
  15. Article
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  17. The role ofiScience · 2022
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  18. Genetic Screening ofFrontiers in microbiology · 2022
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  19. SAGA Complex Subunits inFrontiers in cellular and infection microbiology · 2022
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43 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.

Vincent M BrunoIntegrated Program in Cellular, Molecular, and Biophysical Studies, Columbia University, New York, New York, USA.
Sergey Kalachikov
Ryan Subaran
Clarissa J Nobile
Christos Kyratsous
Aaron P Mitchell
Columbia University · USNew York Genome Center · US

Funding

TRAINING PROGRAM IN MICROBIOLOGY FOR INFECTIOUS DISEASEST32AI007161 · NIAID · COLUMBIA UNIV NEW YORK MORNINGSIDE · PI FIDOCK, DAVID A · 1985 to 2008
$1.9M
C. albicans Regulatory Pathways in Oral CandidiasisR01AI050931 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MITCHELL, AARON P · 2001 to 2005
$1.5M
New strategies for identification of C. albicans fluconazole resistance geneR21AI055823 · NIAID · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI MITCHELL, AARON P · 2003 to 2004
$481k
NIAID NIH HHS R01 AI050931NIAID NIH HHS R01AI050931NIAID NIH HHS R21 AI055823NIAID NIH HHS R21AI055823NIAID NIH HHS T32 AI007161NIAID NIH HHS T32AI07161
6 · The paper itself

Abstract

The fungal cell wall is vital for growth, development, and interaction of cells with their environment. The response to cell wall damage is well understood from studies in the budding yeast Saccharomyces cerevisiae, where numerous cell wall integrity (CWI) genes are activated by transcription factor ScRlm1. Prior evidence suggests the hypothesis that both response and regulation may be conserved in the major fungal pathogen Candida albicans. We have tested this hypothesis by using a new C. albicans genetic resource: we have screened mutants defective in putative transcription factor genes for sensitivity to the cell wall biosynthesis inhibitor caspofungin. We find that the zinc finger protein CaCas5, which lacks a unique ortholog in S. cerevisiae, governs expression of many CWI genes. CaRlm1 has a modest role in this response. The transcriptional coactivator CaAda2 is also required for expression of many CaCas5-dependent genes, as expected if CaCas5 recruits CaAda2 to activate target gene transcription. Many caspofungin-induced C. albicans genes specify endoplasmic reticulum and secretion functions. Such genes are not induced in S. cerevisiae, but promote its growth in caspofungin. We have used a new resource to identify a key C. albicans transcriptional regulator of CWI genes and antifungal sensitivity. Our gene expression findings indicate that both divergent and conserved response genes may have significant functional roles. Our strategy may be broadly useful for identification of pathogen-specific regulatory pathways and critical response genes.

Indexed as

Antifungal AgentsCandida albicansCaspofunginCell WallEchinocandinsGenesLipopeptidesMutationPeptides, CyclicTranscription FactorsTranscription, GeneticAntifungal AgentsCas5 protein, Candida albicansCaspofunginEchinocandinsLipopeptidesPeptides, CyclicTranscription Factors

Identifiers

PMID16552442
PMCPMC1401495
OpenAlexW2079004458

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.