---
res:
  bibo_abstract:
  - The ability to detect and respond to acute oxygen (O2) shortages is indispensable
    to aerobic life. The molecular mechanisms and circuits underlying this capacity
    are poorly understood. Here, we characterize the behavioral responses of feeding
    Caenorhabditis elegans to approximately 1% O2. Acute hypoxia triggers a bout of
    turning maneuvers followed by a persistent switch to rapid forward movement as
    animals seek to avoid and escape hypoxia. While the behavioral responses to 1%
    O2 closely resemble those evoked by 21% O2, they have distinct molecular and circuit
    underpinnings. Disrupting phosphodiesterases (PDEs), specific G proteins, or BBSome
    function inhibits escape from 1% O2 due to increased cGMP signaling. A primary
    source of cGMP is GCY-28, the ortholog of the atrial natriuretic peptide (ANP)
    receptor. cGMP activates the protein kinase G EGL-4 and enhances neuroendocrine
    secretion to inhibit acute responses to 1% O2. Triggering a rise in cGMP optogenetically
    in multiple neurons, including AIA interneurons, rapidly and reversibly inhibits
    escape from 1% O2. Ca2+ imaging reveals that a 7% to 1% O2 stimulus evokes a Ca2+
    decrease in several neurons. Defects in mitochondrial complex I (MCI) and mitochondrial
    complex I (MCIII), which lead to persistently high reactive oxygen species (ROS),
    abrogate acute hypoxia responses. In particular, repressing the expression of
    isp-1, which encodes the iron sulfur protein of MCIII, inhibits escape from 1%
    O2 without affecting responses to 21% O2. Both genetic and pharmacological up-regulation
    of mitochondrial ROS increase cGMP levels, which contribute to the reduced hypoxia
    responses. Our results implicate ROS and precise regulation of intracellular cGMP
    in the modulation of acute responses to hypoxia by C. elegans.@eng
  bibo_authorlist:
  - foaf_Person:
      foaf_givenName: Lina
      foaf_name: Zhao, Lina
      foaf_surname: Zhao
  - foaf_Person:
      foaf_givenName: Lorenz A.
      foaf_name: Fenk, Lorenz A.
      foaf_surname: Fenk
  - foaf_Person:
      foaf_givenName: Lars
      foaf_name: Nilsson, Lars
      foaf_surname: Nilsson
  - foaf_Person:
      foaf_givenName: Niko Paresh
      foaf_name: Amin-Wetzel, Niko Paresh
      foaf_surname: Amin-Wetzel
      foaf_workInfoHomepage: http://www.librecat.org/personId=E95D3014-9D8C-11E9-9C80-D2F8E5697425
  - foaf_Person:
      foaf_givenName: Nelson
      foaf_name: Ramirez, Nelson
      foaf_surname: Ramirez
      foaf_workInfoHomepage: http://www.librecat.org/personId=39831956-E4FE-11E9-85DE-0DC7E5697425
  - foaf_Person:
      foaf_givenName: Mario
      foaf_name: De Bono, Mario
      foaf_surname: De Bono
      foaf_workInfoHomepage: http://www.librecat.org/personId=4E3FF80E-F248-11E8-B48F-1D18A9856A87
    orcid: 0000-0001-8347-0443
  - foaf_Person:
      foaf_givenName: Changchun
      foaf_name: Chen, Changchun
      foaf_surname: Chen
  bibo_doi: 10.1371/journal.pbio.3001684
  bibo_issue: '6'
  bibo_volume: 20
  dct_date: 2022^xs_gYear
  dct_identifier:
  - UT:000828679600001
  dct_isPartOf:
  - http://id.crossref.org/issn/1545-7885
  dct_language: eng
  dct_publisher: Public Library of Science@
  dct_title: ROS and cGMP signaling modulate persistent escape from hypoxia in Caenorhabditis
    elegans@
  fabio_hasPubmedId: '35727855'
...