Evidence map›Paper›PMID 30514845›Full record

ArticleNature communications2018

Neurohormonal signaling via a sulfotransferase antagonizes insulin-like signaling to regulate a Caenorhabditis elegans stress response.

Nicholas O Burton, Vivek K Dwivedi, Kirk B Burkhart, Rebecca E W Kaplan, L Ryan Baugh, H Robert Horvitz

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 26% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. OSM-11 modulates salinity-stress tolerance inbioRxiv : the preprint server for biology · 2025
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  5. Oocyte mitochondria link maternal environment to offspring phenotype.bioRxiv : the preprint server for biology · 2025
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  8. The lipidomes ofAging · 2023
    Article
  9. Article
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  11. Review
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
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 2 countries.

Nicholas O BurtonHoward Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. nob20@cam.ac.uk.
Vivek K DwivediHoward Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Kirk B BurkhartHoward Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA.
Rebecca E W KaplanDepartment of Biology, Duke University, Durham, NC, 27708, USA.
L Ryan BaughDepartment of Biology, Duke University, Durham, NC, 27708, USA.ORCID http://orcid.org/0000-0003-2148-5492
H Robert HorvitzHoward Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, MA, 02139, USA. horvitz@mit.edu.
Howard Hughes Medical Institute · USDuke University · US

Funding

Genetic Analysis of Nematode Egg Laying and Co-regulated Behavioral SystemsR01GM024663 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI HORVITZ, H ROBERT · 1985 to 2025
$10.1M
Genetics Training Grant-Year 26T32GM007754 · NIGMS · DUKE UNIVERSITY · PI HAASE, STEVEN B · 1985 to 2019
$8.3M
Systemic, maternal and transgenerational effects of nutrient stressR01GM117408 · NIGMS · DUKE UNIVERSITY · PI BAUGH, LARRY RYAN · 2015 to 2022
$2.5M
GENETIC ANALYSIS OF NEMATODE EGG-LAYINGR37GM024663 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI HORVITZ, H R · 1991 to 2000
$363k
NIGMS NIH HHS R01 GM024663NIGMS NIH HHS R01 GM117408NIGMS NIH HHS R37 GM024663
6 · The paper itself

Abstract

Insulin and insulin-like signaling regulates a broad spectrum of growth and metabolic responses to a variety of internal and environmental stimuli. For example, the inhibition of insulin-like signaling in C. elegans mediates its response to both osmotic stress and starvation. We report that in response to osmotic stress the cytosolic sulfotransferase SSU-1 antagonizes insulin-like signaling and promotes developmental arrest. Both SSU-1 and the DAF-16 FOXO transcription factor, which is activated when insulin signaling is low, are needed to drive specific responses to reduced insulin-like signaling. We demonstrate that SSU-1 functions in a single pair of sensory neurons to control intercellular signaling via the nuclear hormone receptor NHR-1 and promote both the specific transcriptional response to osmotic stress and altered lysophosphatidylcholine metabolism. Our results show the requirement of a sulfotransferase-nuclear hormone receptor neurohormonal signaling pathway for some but not all consequences of reduced insulin-like signaling.

Indexed as

AnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsCloning, MolecularEmbryonic DevelopmentEmbryo, NonmammalianForkhead Transcription FactorsGene Expression Regulation, DevelopmentalInsulinLysophosphatidylcholinesMutagenesisNerve Tissue ProteinsNeurotransmitter AgentsOsmotic PressureReceptor, InsulinReceptors, Cytoplasmic and NuclearCaenorhabditis elegans Proteinsdaf-16 protein, C elegansForkhead Transcription FactorsInsulinLysophosphatidylcholinesNerve Tissue ProteinsNeurotransmitter AgentsReceptor, InsulinReceptors, Cytoplasmic and NuclearRNA, MessengerSSU-1 protein, C elegansSulfotransferases

Identifiers

PMID30514845
PMCPMC6279808
OpenAlexW2902096271

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.