1. Neuroscience

Control of feeding by Piezo-mediated gut mechanosensation in Drosophila

  1. Soohong Min
  2. Yangkyun Oh
  3. Pushpa Verma
  4. Samuel C Whitehead
  5. Nilay Yapici
  6. David Van Vactor
  7. Greg SB Suh
  8. Stephen Liberles  Is a corresponding author
  1. Harvard Medical School, United States
  2. Skirball Institute, NYU, United States
  3. Cornell University, United States
https://doi.org/10.7554/eLife.63049
Share this article
Cite this article
  1. Soohong Min
  2. Yangkyun Oh
  3. Pushpa Verma
  4. Samuel C Whitehead
  5. Nilay Yapici
  6. David Van Vactor
  7. Greg SB Suh
  8. Stephen Liberles
(2021)
Control of feeding by Piezo-mediated gut mechanosensation in Drosophila
eLife 10:e63049.
https://doi.org/10.7554/eLife.63049
  2. Download BibTeX
  3. Download .RIS

Abstract

Across animal species, meals are terminated after ingestion of large food volumes, yet underlying mechanosensory receptors have so far remained elusive. Here, we identify an essential role for Drosophila Piezo in volume-based control of meal size. We discover a rare population of fly neurons that express Piezo, innervate the anterior gut and crop (a food reservoir organ), and respond to tissue distension in a Piezo-dependent manner. Activating Piezo neurons decreases appetite, while Piezo knockout and Piezo neuron silencing cause gut bloating and increase both food consumption and body weight. These studies reveal that disrupting gut distension receptors changes feeding patterns, and identify a key role for Drosophila Piezo in internal organ mechanosensation.

Data availability

All datapoints used are provided in Figures and in a Source Data File.

Article and author information

Author details

  1. Soohong Min

    Cell Biology, Harvard Medical School, Boston, United States
    Competing interests
    No competing interests declared.

  2. Yangkyun Oh

    Molecular Neurobiology, Skirball Institute, NYU, New York, United States
    Competing interests
    No competing interests declared.

  3. Pushpa Verma

    Cell Biology, Harvard Medical School, Boston, United States
    Competing interests
    No competing interests declared.

  4. Samuel C Whitehead

    Physics, Cornell University, Ithaca, NY, United States
    Competing interests
    No competing interests declared.

  5. Nilay Yapici

    Department of Neurobiology and Behavior, Cornell University, Ithaca, United States
    Competing interests
    No competing interests declared.

  6. David Van Vactor

    Department of Cell Biology, Harvard Medical School, Boston, United States
    Competing interests
    No competing interests declared.

  7. Greg SB Suh

    Molecular Neurobiology, Skirball Institute, NYU, New York, United States
    Competing interests
    No competing interests declared.

  8. Stephen Liberles

    Department of Cell Biology, Harvard Medical School, Boston, United States
    For correspondence
    Stephen_Liberles@hms.harvard.edu
    Competing interests
    Stephen Liberles, Reviewing editor, eLife.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-2177-9741

Funding

American Heart Association (20POST35210914)

  • Soohong Min

National Institutes of Health (NS090994)

  • David Van Vactor

National Institutes of Health (RO1DK116294)

  • Greg SB Suh

National Institutes of Health (RO1DK106636)

  • Greg SB Suh

Samsung Science and Technology Foundation (SSTF-BA-1802-11)

  • Greg SB Suh

Howard Hughes Medical Institute

  • Stephen Liberles

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Copyright

© 2021, Min et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

Metrics

  • 5,937
    views
  • 795
    downloads
  • 51
    citations

Views, downloads and citations are aggregated across all versions of this paper published by eLife.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Open citations (links to open the citations from this article in various online reference manager services)

Cite this article (links to download the citations from this article in formats compatible with various reference manager tools)

  1. Soohong Min
  2. Yangkyun Oh
  3. Pushpa Verma
  4. Samuel C Whitehead
  5. Nilay Yapici
  6. David Van Vactor
  7. Greg SB Suh
  8. Stephen Liberles
(2021)
Control of feeding by Piezo-mediated gut mechanosensation in Drosophila
eLife 10:e63049.
https://doi.org/10.7554/eLife.63049

Share this article

https://doi.org/10.7554/eLife.63049

Categories and tags

Research organism

Further reading

    1. Neuroscience

    Parabrachial CGRP neurons modulate active defensive behavior under a naturalistic threat

    Gyeong Hee Pyeon, Hyewon Cho ... Yong Sang Jo
    Research Article Updated

    Recent studies suggest that calcitonin gene-related peptide (CGRP) neurons in the parabrachial nucleus (PBN) represent aversive information and signal a general alarm to the forebrain. If CGRP neurons serve as a true general alarm, their activation would modulate both passive nad active defensive behaviors depending on the magnitude and context of the threat. However, most prior research has focused on the role of CGRP neurons in passive freezing responses, with limited exploration of their involvement in active defensive behaviors. To address this, we examined the role of CGRP neurons in active defensive behavior using a predator-like robot programmed to chase mice. Our electrophysiological results revealed that CGRP neurons encode the intensity of aversive stimuli through variations in firing durations and amplitudes. Optogenetic activation of CGRP neurons during robot chasing elevated flight responses in both conditioning and retention tests, presumably by amplifying the perception of the threat as more imminent and dangerous. In contrast, animals with inactivated CGRP neurons exhibited reduced flight responses, even when the robot was programmed to appear highly threatening during conditioning. These findings expand the understanding of CGRP neurons in the PBN as a critical alarm system, capable of dynamically regulating active defensive behaviors by amplifying threat perception, and ensuring adaptive responses to varying levels of danger.

    1. Neuroscience

    Disruption of the CRF1 receptor eliminates morphine-induced sociability deficits and firing of oxytocinergic neurons in male mice

    Alessandro Piccin, Anne-Emilie Allain ... Angelo Contarino
    Research Article

    Substance-induced social behavior deficits dramatically worsen the clinical outcome of substance use disorders; yet, the underlying mechanisms remain poorly understood. Herein, we investigated the role for the corticotropin-releasing factor receptor 1 (CRF1) in the acute sociability deficits induced by morphine and the related activity of oxytocin (OXY)- and arginine-vasopressin (AVP)-expressing neurons of the paraventricular nucleus of the hypothalamus (PVN). For this purpose, we used both the CRF1 receptor-preferring antagonist compound antalarmin and the genetic mouse model of CRF1 receptor-deficiency. Antalarmin completely abolished sociability deficits induced by morphine in male, but not in female, C57BL/6J mice. Accordingly, genetic CRF1 receptor-deficiency eliminated morphine-induced sociability deficits in male mice. Ex vivo electrophysiology studies showed that antalarmin also eliminated morphine-induced firing of PVN neurons in male, but not in female, C57BL/6J mice. Likewise, genetic CRF1 receptor-deficiency reduced morphine-induced firing of PVN neurons in a CRF1 gene expression-dependent manner. The electrophysiology results consistently mirrored the behavioral results, indicating a link between morphine-induced PVN activity and sociability deficits. Interestingly, in male mice antalarmin abolished morphine-induced firing in neurons co-expressing OXY and AVP, but not in neurons expressing only AVP. In contrast, in female mice antalarmin did not affect morphine-induced firing of neurons co-expressing OXY and AVP or only OXY, indicating a selective sex-specific role for the CRF1 receptor in opiate-induced PVN OXY activity. The present findings demonstrate a major, sex-linked, role for the CRF1 receptor in sociability deficits and related brain alterations induced by morphine, suggesting new therapeutic strategy for opiate use disorders.

    1. Evolutionary Biology
    2. Neuroscience

    Vision: The inner workings of a miniature eye

    Gregor Belušič
    Insight

    The first complete 3D reconstruction of the compound eye of a minute wasp species sheds light on the nuts and bolts of size reduction.