Evidence map›Paper›PMID 28423062›Full record

ArticlePLoS pathogens2017

Filamentous fungal carbon catabolite repression supports metabolic plasticity and stress responses essential for disease progression.

Sarah R Beattie, Kenneth M K Mark, Arsa Thammahong, Laure Nicolas Annick Ries, Sourabh Dhingra, Alayna K Caffrey-Carr, Chao Cheng, Candice C Black, Paul Bowyer, Michael J Bromley and 3 more

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing 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

70 citing papers in PubMed, 100 citations in OpenAlex.

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  7. Trans-Kingdom dsRNA Sensing:bioRxiv : the preprint server for biology · 2026
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  13. Whole-chromosome duplications drive antimicrobial resistance inbioRxiv : the preprint server for biology · 2025
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  15. Recent developments inMicrobiology and molecular biology reviews : MMBR · 2025
    Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Review

10 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

13 authors at 4 institutions in 3 countries.

Sarah R BeattieDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.ORCID http://orcid.org/0000-0002-0633-2618
Kenneth M K MarkDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.
Arsa ThammahongDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.ORCID http://orcid.org/0000-0002-0482-4176
Laure Nicolas Annick RiesFaculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Brazil.ORCID http://orcid.org/0000-0001-9653-3159
Sourabh DhingraDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.
Alayna K Caffrey-CarrDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.
Chao ChengDepartment of Molecular and Systems Biology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.
Candice C BlackDepartment of Pathology, Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, United States of America.ORCID http://orcid.org/0000-0002-1808-5263
Paul BowyerManchester Fungal Infection Group, School of Biological Sciences, University of Manchester, Manchester, United Kingdom.ORCID http://orcid.org/0000-0002-1083-9286
Michael J BromleyManchester Fungal Infection Group, School of Biological Sciences, University of Manchester, Manchester, United Kingdom.ORCID http://orcid.org/0000-0002-7611-0201
Joshua J ObarDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.
Gustavo H GoldmanFaculdade de Ciências Farmacêuticas de Ribeirão Preto, Universidade de São Paulo, Brazil.ORCID http://orcid.org/0000-0002-2986-350X
Robert A CramerDepartment of Microbiology and Immunology, Geisel School of Medicine at Dartmouth, Hanover, New Hampshire, United States of America.ORCID http://orcid.org/0000-0001-5503-5006
Dartmouth College · USUniversidade de São Paulo · BRUniversity of Manchester · GBDartmouth–Hitchcock Medical Center · US

Funding

Molecular and Cellular Biology at DartmouthT32GM008704 · NIGMS · DARTMOUTH COLLEGE · PI COMPTON, DUANE A. · 1998 to 2018
$6.8M
TRANSLATIONAL RESEARCH COREP30GM106394 · NIGMS · DARTMOUTH COLLEGE · PI MADDEN, DEAN R · 2013 to 2017
$6.1M
HOST-MICROBE INTERACTIONST32AI007519 · NIAID · DARTMOUTH COLLEGE · PI DEBORAH A HOGAN · 1997 to 2026
$5.9M
Hypoxia Adaptation and Fungal Virulence of Aspergillus fumigatusR01AI081838 · NIAID · MONTANA STATE UNIVERSITY - BOZEMAN · PI CRAMER, ROBERT ANDREW · 2009 to 2017
$2.9M
NIAID NIH HHS R01 AI081838NIAID NIH HHS T32 AI007519NIGMS NIH HHS P30 GM106394NIGMS NIH HHS T32 GM008704
6 · The paper itself

Abstract

Aspergillus fumigatus is responsible for a disproportionate number of invasive mycosis cases relative to other common filamentous fungi. While many fungal factors critical for infection establishment are known, genes essential for disease persistence and progression are ill defined. We propose that fungal factors that promote navigation of the rapidly changing nutrient and structural landscape characteristic of disease progression represent untapped clinically relevant therapeutic targets. To this end, we find that A. fumigatus requires a carbon catabolite repression (CCR) mediated genetic network to support in vivo fungal fitness and disease progression. While CCR as mediated by the transcriptional repressor CreA is not required for pulmonary infection establishment, loss of CCR inhibits fungal metabolic plasticity and the ability to thrive in the dynamic infection microenvironment. Our results suggest a model whereby CCR in an environmental filamentous fungus is dispensable for initiation of pulmonary infection but essential for infection maintenance and disease progression. Conceptually, we argue these data provide a foundation for additional studies on fungal factors required to support fungal fitness and disease progression and term such genes and factors, DPFs (disease progression factors).

Indexed as

Catabolite RepressionGene Regulatory NetworksAspergillosisAspergillus fumigatusCarbonDisease ProgressionFungal ProteinsGene Expression Regulation, FungalModels, BiologicalRepressor ProteinsStress, PhysiologicalCarbonFungal ProteinsRepressor Proteins

Identifiers

PMID28423062
PMCPMC5411099
OpenAlexW2607468292

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.