The balance between cytoplasmic and nuclear CaM kinase-1 signaling controls the operating range of noxious heat avoidance.
- Schild LC Department of Biology, University of Fribourg, 1700 Fribourg, Switzerland.
- Zbinden L Department of Biology, University of Fribourg, 1700 Fribourg, Switzerland.
- Bell HW Department of Biology and National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, USA.
- Yu YV Department of Biology and National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, USA.
- Sengupta P Department of Biology and National Center for Behavioral Genomics, Brandeis University, Waltham, MA 02454, USA.
- Goodman MB Department of Molecular and Cellular Physiology, Stanford School of Medicine, Stanford, CA 94305, USA. Electronic address: mbgoodman@stanford.edu.
- Glauser DA Department of Biology, University of Fribourg, 1700 Fribourg, Switzerland. Electronic address: dominique.glauser@unifr.ch.
- 2014-12-04
Published in:
- Neuron. - 2014
Adaptation, Physiological
Animals
Animals, Genetically Modified
Avoidance Learning
Caenorhabditis elegans
Caenorhabditis elegans Proteins
Calcium-Calmodulin-Dependent Protein Kinase Type 1
Cell Nucleolus
Cytoplasm
Escape Reaction
Hot Temperature
Mutagenesis
Mutation
Neurons
Neuropeptides
Nociception
Sensory Receptor Cells
Signal Transduction
English
Through encounters with predators, competitors, and noxious stimuli, animals have evolved defensive responses that minimize injury and are essential for survival. Physiological adaptation modulates the stimulus intensities that trigger such nocifensive behaviors, but the molecular networks that define their operating range are largely unknown. Here, we identify a gain-of-function allele of the cmk-1 CaMKI gene in C. elegans and show that loss of the regulatory domain of the CaMKI enzyme produces thermal analgesia and shifts the operating range for nocifensive heat avoidance to higher temperatures. Such analgesia depends on nuclear CMK-1 signaling, while cytoplasmic CMK-1 signaling lowers the threshold for thermal avoidance. CMK-1 acts downstream of heat detection in thermal receptor neurons and controls neuropeptide release. Our results establish CaMKI as a key regulator of the operating range for nocifensive behaviors and suggest strategies for producing thermal analgesia through the regulation of CaMKI-dependent signaling.
- Language
-
- English
- Open access status
- bronze
- Identifiers
-
- DOI 10.1016/j.neuron.2014.10.039
- PMID 25467982
- Persistent URL
- https://sonar.ch/global/documents/93529
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