Evidence map›Paper›PMID 30668573›Full record

ArticlePLoS genetics2019

The nuclear hormone receptor NHR-86 controls anti-pathogen responses in C. elegans.

Nicholas D Peterson, Hilary K Cheesman, Pengpeng Liu, Sarah M Anderson, Kyle J Foster, Richa Chhaya, Paola Perrat, Jose Thekkiniath, Qiyuan Yang, Cole M Haynes and 1 more

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.

0numbers the graph read from it
0cells of the map it votes in
39citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

39 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  3. bioRxiv : the preprint server for biology · 2026
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  11. Unzipping the defense: a comprehensive review on bZIP transcription factors inFrontiers in cellular and infection microbiology · 2025
    Review
  12. Article
  13. Article
  14. Modeling Host-Pathogen Interactions inInternational journal of molecular sciences · 2024
    Review
  15. Article
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  17. 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

11 authors at 1 institution in 1 country.

Nicholas D PetersonProgram in Innate Immunity, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, United States of America.
Hilary K CheesmanProgram in Innate Immunity, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, United States of America.ORCID 0000-0001-7582-9698
Pengpeng LiuDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, United States of America.ORCID 0000-0002-4891-8780
Sarah M AndersonProgram in Innate Immunity, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, United States of America.
Kyle J FosterProgram in Innate Immunity, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, United States of America.ORCID 0000-0002-6385-6215
Richa ChhayaProgram in Innate Immunity, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, United States of America.ORCID 0000-0002-5108-5564
Paola PerratDepartment of Neurobiology, University of Massachusetts Medical School, Worcester, MA, United States of America.
Jose ThekkiniathProgram in Innate Immunity, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, United States of America.
Qiyuan YangDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, United States of America.
Cole M HaynesDepartment of Molecular, Cell and Cancer Biology, University of Massachusetts Medical School, Worcester, MA, United States of America.
Read Pukkila-WorleyProgram in Innate Immunity, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, United States of America.ORCID 0000-0001-5340-8294
University of Massachusetts Chan Medical School · US

Funding

Enhancing and expanding the CGC Strain CollectionP40OD010440 · OD · UNIVERSITY OF MINNESOTA · PI Aric L Daul, Ann E. Rougvie · 2012 to 2026
$7.5M
An Immune Surveillance Network in C. elegansR01AI130289 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI PUKKILA-WORLEY, READ · 2017 to 2025
$4.6M
TRAINING IN IMMUNOLOGY (COMPETITIVE RENEWAL OF AI07439)T32AI007349 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI STERN, LAWRENCE J. · 1989 to 2024
$4.5M
Innate Immunity Training ProgramT32AI095213 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI SILVERMAN, NEAL · 2011 to 2025
$2.5M
Coordinated Repair and Regeneration of Defective MitochondriaR01AG047182 · NIA · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HAYNES, COLE M · 2015 to 2019
$2.1M
Training in the Molecular Basis of Autoimmunity and AutoinflammationT32AI132152 · NIAID · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI Katherine A. Fitzgerald, Ann Marshak-Rothstein · 2018 to 2026
$1.6M
NIAID NIH HHS R01 AI130289NIAID NIH HHS T32 AI007349NIAID NIH HHS T32 AI095213NIAID NIH HHS T32 AI132152NIA NIH HHS R01 AG047182NIH HHS P40 OD010440
6 · The paper itself

Abstract

Nuclear hormone receptors (NHRs) are ligand-gated transcription factors that control adaptive host responses following recognition of specific endogenous or exogenous ligands. Although NHRs have expanded dramatically in C. elegans compared to other metazoans, the biological function of only a few of these genes has been characterized in detail. Here, we demonstrate that an NHR can activate an anti-pathogen transcriptional program. Using genetic epistasis experiments, transcriptome profiling analyses and chromatin immunoprecipitation-sequencing, we show that, in the presence of an immunostimulatory small molecule, NHR-86 binds to the promoters of immune effectors to activate their transcription. NHR-86 is not required for resistance to the bacterial pathogen Pseudomonas aeruginosa at baseline, but activation of NHR-86 by this compound drives a transcriptional program that provides protection against this pathogen. Interestingly, NHR-86 targets immune effectors whose basal regulation requires the canonical p38 MAPK PMK-1 immune pathway. However, NHR-86 functions independently of PMK-1 and modulates the transcription of these infection response genes directly. These findings characterize a new transcriptional regulator in C. elegans that can induce a protective host response towards a bacterial pathogen.

Indexed as

Amino Acid SequenceAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsGene Expression RegulationImmunity, InnateMitogen-Activated Protein KinasesMutationp38 Mitogen-Activated Protein KinasesPseudomonas aeruginosaReceptors, Cytoplasmic and NuclearCaenorhabditis elegans ProteinsMitogen-Activated Protein KinasesNHR-86 protein, C elegansp38 Mitogen-Activated Protein KinasesPmk-1 protein, C elegansReceptors, Cytoplasmic and Nuclear

Identifiers

PMID30668573
PMCPMC6358101
OpenAlexW2911766507

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.