Evidence map›Paper›PMID 20824071›Full record

ArticlePLoS genetics2010

Response to mechanical stress is mediated by the TRPA channel painless in the Drosophila heart.

Sébastien Sénatore, Vatrapu Rami Reddy, Michel Sémériva, Laurent Perrin, Nathalie Lalevée

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.1field-weighted citation impact, top 28% 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

23 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Mending a broken heart:Disease models & mechanisms · 2021
    Review
  7. Article
  8. Article
  9. Using optogenetics to assess neuroendocrine modulation of heart rate in Drosophila melanogaster larvae.Journal of comparative physiology. A, Neuroethology, sensory, neural, and behavioral physiology · 2017
    Article
  10. Article
  11. Article
  12. On the Morphology of the Drosophila Heart.Journal of cardiovascular development and disease · 2016
    Review
  13. Probing the Electrophysiology of the Developing Heart.Journal of cardiovascular development and disease · 2016
    Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Article
  19. Mechanobiology in cardiac physiology and diseases.Journal of cellular and molecular medicine · 2013
    Review
  20. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Sébastien SénatoreInstitut de Biologie du Développement de Marseille-Luminy, UMR-CNRS 6216, Université de la Méditerranée, Marseille, France.
Vatrapu Rami Reddy
Michel Sémériva
Laurent Perrin
Nathalie Lalevée
Institut de Biologie du Développement Marseille · FRCentre National de la Recherche Scientifique · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mechanotransduction modulates cellular functions as diverse as migration, proliferation, differentiation, and apoptosis. It is crucial for organ development and homeostasis and leads to pathologies when defective. However, despite considerable efforts made in the past, the molecular basis of mechanotransduction remains poorly understood. Here, we have investigated the genetic basis of mechanotransduction in Drosophila. We show that the fly heart senses and responds to mechanical forces by regulating cardiac activity. In particular, pauses in heart activity are observed under acute mechanical constraints in vivo. We further confirm by a variety of in situ tests that these cardiac arrests constitute the biological force-induced response. In order to identify molecular components of the mechanotransduction pathway, we carried out a genetic screen based on the dependence of cardiac activity upon mechanical constraints and identified Painless, a TRPA channel. We observe a clear absence of in vivo cardiac arrest following inactivation of painless and further demonstrate that painless is autonomously required in the heart to mediate the response to mechanical stress. Furthermore, direct activation of Painless is sufficient to produce pauses in heartbeat, mimicking the pressure-induced response. Painless thus constitutes part of a mechanosensitive pathway that adjusts cardiac muscle activity to mechanical constraints. This constitutes the first in vivo demonstration that a TRPA channel can mediate cardiac mechanotransduction. Furthermore, by establishing a high-throughput system to identify the molecular players involved in mechanotransduction in the cardiovascular system, our study paves the way for understanding the mechanisms underlying a mechanotransduction pathway.

Indexed as

Stress, MechanicalAnimalsDrosophila melanogasterDrosophila ProteinsGene Knockdown TechniquesGenetic TestingIon Channel GatingIon ChannelsLarvaMechanotransduction, CellularMyocardiumTemperatureDrosophila ProteinsIon Channelspain protein, Drosophila

Identifiers

PMID20824071
PMCPMC2932686
OpenAlexW1991389269

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.