Evidence map›Paper›PMID 20176974›Full record

ArticleGenetics2010

Caenorhabditis elegans TRPV channels function in a modality-specific pathway to regulate response to aberrant sensory signaling.

Meredith J Ezak, Elizabeth Hong, Angela Chaparro-Garcia, Denise M Ferkey

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
0.6field-weighted citation impact, top 39% 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

20 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
  2. Article
  3. Chemosensory adaptations inBiology letters · 2025
    Article
  4. Article
  5. Article
  6. Article
  7. Phosphodiesterases RegulatemicroPublication biology · 2025
    Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. ThemicroPublication biology · 2020
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Circadian regulation of olfaction and an evolutionarily conserved, nontranscriptional marker in Caenorhabditis elegans.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  18. Article
  19. Article
  20. 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

4 authors at 1 institution in 1 country.

Meredith J EzakDepartment of Biological Sciences, State University of New York, Buffalo, NY 14260, USA.
Elizabeth Hong
Angela Chaparro-Garcia
Denise M Ferkey
University at Buffalo, State University of New York · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Olfaction and some forms of taste (including bitter) are mediated by G protein-coupled signal transduction pathways. Olfactory and gustatory ligands bind to chemosensory G protein-coupled receptors (GPCRs) in specialized sensory cells to activate intracellular signal transduction cascades. G protein-coupled receptor kinases (GRKs) are negative regulators of signaling that specifically phosphorylate activated GPCRs to terminate signaling. Although loss of GRK function usually results in enhanced cellular signaling, Caenorhabditis elegans lacking GRK-2 function are not hypersensitive to chemosensory stimuli. Instead, grk-2 mutant animals do not chemotax toward attractive olfactory stimuli or avoid aversive tastes and smells. We show here that loss-of-function mutations in the transient receptor potential vanilloid (TRPV) channels OSM-9 and OCR-2 selectively restore grk-2 behavioral avoidance of bitter tastants, revealing modality-specific mechanisms for TRPV channel function in the regulation of C. elegans chemosensation. Additionally, a single amino acid point mutation in OCR-2 that disrupts TRPV channel-mediated gene expression, but does not decrease channel function in chemosensory primary signal transduction, also restores grk-2 bitter taste avoidance. Thus, loss of GRK-2 function may lead to changes in gene expression, via OSM-9/OCR-2, to selectively alter the levels of signaling components that transduce or regulate bitter taste responses. Our results suggest a novel mechanism and multiple modality-specific pathways that sensory cells employ in response to aberrant signal transduction.

Indexed as

Signal TransductionAnimalsCaenorhabditis elegansCaenorhabditis elegans ProteinsChemotaxisIon ChannelsMutationNerve Tissue ProteinsPoint MutationQuinineSensationSensory Receptor CellsTasteTransient Receptor Potential ChannelsTRPV Cation ChannelsCaenorhabditis elegans ProteinsIon ChannelsNerve Tissue ProteinsOCR-2 protein, C elegansOSM-9 protein, C elegansQuinineTransient Receptor Potential ChannelsTRPV Cation Channels

Identifiers

PMID20176974
PMCPMC2870959
OpenAlexW2149655225

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.