Abstract
Carbon dioxide (CO2) is a key molecule in many biological processes; however, mechanisms by which organisms sense and respond to high CO2 levels remain largely unknown. Here we report that acute CO2 exposure leads to a rapid cessation in the contraction of the pharynx muscles in Caenorhabditis elegans. To uncover the molecular mechanisms underlying this response, we performed a forward genetic screen and found that hid-1, a key component in neuropeptide signaling, regulates this inhibition in muscle contraction. Surprisingly, we found that this hid-1-mediated pathway is independent of any previously known pathways controlling CO2 avoidance and oxygen sensing. In addition, animals with mutations in unc-31 and egl-21 (neuropeptide secretion and maturation components) show impaired inhibition of muscle contraction following acute exposure to high CO2 levels, in further support of our findings. Interestingly, the observed response in the pharynx muscle requires the BAG neurons, which also mediate CO2 avoidance. This novel hid-1-mediated pathway sheds new light on the physiological effects of high CO2 levels on animals at the organism-wide level.
Original language | American English |
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Article number | e1004529 |
Journal | PLoS Genetics |
Volume | 10 |
Issue number | 8 |
DOIs | |
State | Published - 7 Aug 2014 |
Bibliographical note
Funding Information:Funding: This work was supported by the Arian Solis Ostrosky and Sydney Dwyer Davis foundation to YG and the NIH RO1-HL85534 to JIS and YG. Funding was also received from the European Research Council under the European Union’s Seventh Framework Programme (FP/2007-2013)/ERC Grant Nu 336803 to AZ. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Funding Information:
This work was supported by the Arian Solis Ostrosky and Sydney Dwyer Davis foundation to YG and the NIH RO1-HL85534 to JIS and YG. Funding was also received from the European Research Council under the European Union?s Seventh Framework Programme (FP/2007-2013)/ERC Grant Nu 336803 to AZ. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Publisher Copyright:
© 2014 Sharabi et al.