The response to high CO2 levels requires the neuropeptide secretion component HID-1 to promote pumping inhibition.
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 elega...
| Main Authors: | , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Public Library of Science (PLoS)
2014-08-01
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| Series: | PLoS Genetics |
| Online Access: | http://europepmc.org/articles/PMC4125093?pdf=render |
| _version_ | 1819131694719959040 |
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| author | Kfir Sharabi Chayki Charar Nurit Friedman Inbar Mizrahi Alon Zaslaver Jacob I Sznajder Yosef Gruenbaum |
| author_facet | Kfir Sharabi Chayki Charar Nurit Friedman Inbar Mizrahi Alon Zaslaver Jacob I Sznajder Yosef Gruenbaum |
| author_sort | Kfir Sharabi |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-22T09:19:35Z |
| format | Article |
| id | doaj.art-6e0bcdfb7fa54852a48f733d6fb3690a |
| institution | Directory Open Access Journal |
| issn | 1553-7390 1553-7404 |
| language | English |
| last_indexed | 2024-12-22T09:19:35Z |
| publishDate | 2014-08-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS Genetics |
| spelling | doaj.art-6e0bcdfb7fa54852a48f733d6fb3690a2022-12-21T18:31:13ZengPublic Library of Science (PLoS)PLoS Genetics1553-73901553-74042014-08-01108e100452910.1371/journal.pgen.1004529The response to high CO2 levels requires the neuropeptide secretion component HID-1 to promote pumping inhibition.Kfir SharabiChayki ChararNurit FriedmanInbar MizrahiAlon ZaslaverJacob I SznajderYosef GruenbaumCarbon 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.http://europepmc.org/articles/PMC4125093?pdf=render |
| spellingShingle | Kfir Sharabi Chayki Charar Nurit Friedman Inbar Mizrahi Alon Zaslaver Jacob I Sznajder Yosef Gruenbaum The response to high CO2 levels requires the neuropeptide secretion component HID-1 to promote pumping inhibition. PLoS Genetics |
| title | The response to high CO2 levels requires the neuropeptide secretion component HID-1 to promote pumping inhibition. |
| title_full | The response to high CO2 levels requires the neuropeptide secretion component HID-1 to promote pumping inhibition. |
| title_fullStr | The response to high CO2 levels requires the neuropeptide secretion component HID-1 to promote pumping inhibition. |
| title_full_unstemmed | The response to high CO2 levels requires the neuropeptide secretion component HID-1 to promote pumping inhibition. |
| title_short | The response to high CO2 levels requires the neuropeptide secretion component HID-1 to promote pumping inhibition. |
| title_sort | response to high co2 levels requires the neuropeptide secretion component hid 1 to promote pumping inhibition |
| url | http://europepmc.org/articles/PMC4125093?pdf=render |
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