Antagonist actions of CMK-1/CaMKI and TAX-6/calcineurin along the C. elegans thermal avoidance circuit orchestrate adaptation of nociceptive response to repeated stimuli

Thermal nociception in Caenorhabditis elegans is regulated by the Ca²+/calmodulin-dependent protein kinase CMK-1, but its downstream effectors have remained unclear. Here, we combined in vitro kinase assays with mass-spectrometry-based phosphoproteomics to identify hundreds of CMK-1 substrates, incl...

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Main Authors: Martina Rudgalvyte, Zehan Hu, Dieter Kressler, Jörn Dengjel, Dominique A Glauser
Format: Article
Language:English
Published: eLife Sciences Publications Ltd 2025-04-01
Series:eLife
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Online Access:https://elifesciences.org/articles/103497
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author Martina Rudgalvyte
Zehan Hu
Dieter Kressler
Jörn Dengjel
Dominique A Glauser
author_facet Martina Rudgalvyte
Zehan Hu
Dieter Kressler
Jörn Dengjel
Dominique A Glauser
author_sort Martina Rudgalvyte
collection DOAJ
description Thermal nociception in Caenorhabditis elegans is regulated by the Ca²+/calmodulin-dependent protein kinase CMK-1, but its downstream effectors have remained unclear. Here, we combined in vitro kinase assays with mass-spectrometry-based phosphoproteomics to identify hundreds of CMK-1 substrates, including the calcineurin A subunit TAX-6, phosphorylated within its conserved regulatory domain. Genetic and pharmacological analyses reveal multiple antagonistic interactions between CMK-1 and calcineurin signaling in modulating both naive thermal responsiveness and adaptation to repeated noxious stimuli. Cell-specific manipulations indicate that CMK-1 acts in AFD and ASER thermo-sensory neurons, while TAX-6 functions in FLP thermo-sensory neurons and downstream interneurons. Since CMK-1 and TAX-6 act in distinct cell types, the phosphorylation observed in vitro might not directly underlie the behavioral phenotype. Instead, the opposing effects seem to arise from their distributed roles within the sensory circuit. Overall, our study provides (1) a resource of candidate CMK-1 targets for further dissecting CaM kinase signaling and (2) evidence of a previously unrecognized, circuit-level antagonism between CMK-1 and calcineurin pathways. These findings highlight a complex interplay of signaling modules that modulate thermal nociception and adaptation, offering new insights into potentially conserved mechanisms that shape nociceptive plasticity and pain (de)sensitization in more complex nervous systems.
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spelling doaj-art-5541280c16104367b9a18fc4706e44bf2025-08-20T02:55:44ZengeLife Sciences Publications LtdeLife2050-084X2025-04-011410.7554/eLife.103497Antagonist actions of CMK-1/CaMKI and TAX-6/calcineurin along the C. elegans thermal avoidance circuit orchestrate adaptation of nociceptive response to repeated stimuliMartina Rudgalvyte0https://orcid.org/0009-0003-6201-6200Zehan Hu1Dieter Kressler2https://orcid.org/0000-0003-4855-3563Jörn Dengjel3https://orcid.org/0000-0002-9453-4614Dominique A Glauser4https://orcid.org/0000-0002-3228-7304Department of Biology, University of Fribourg, Fribourg, SwitzerlandDepartment of Biology, University of Fribourg, Fribourg, SwitzerlandDepartment of Biology, University of Fribourg, Fribourg, Switzerland; Metabolomics and Proteomics Platform (MAPP), Department of Biology, University of Fribourg, Fribourg, SwitzerlandDepartment of Biology, University of Fribourg, Fribourg, SwitzerlandDepartment of Biology, University of Fribourg, Fribourg, SwitzerlandThermal nociception in Caenorhabditis elegans is regulated by the Ca²+/calmodulin-dependent protein kinase CMK-1, but its downstream effectors have remained unclear. Here, we combined in vitro kinase assays with mass-spectrometry-based phosphoproteomics to identify hundreds of CMK-1 substrates, including the calcineurin A subunit TAX-6, phosphorylated within its conserved regulatory domain. Genetic and pharmacological analyses reveal multiple antagonistic interactions between CMK-1 and calcineurin signaling in modulating both naive thermal responsiveness and adaptation to repeated noxious stimuli. Cell-specific manipulations indicate that CMK-1 acts in AFD and ASER thermo-sensory neurons, while TAX-6 functions in FLP thermo-sensory neurons and downstream interneurons. Since CMK-1 and TAX-6 act in distinct cell types, the phosphorylation observed in vitro might not directly underlie the behavioral phenotype. Instead, the opposing effects seem to arise from their distributed roles within the sensory circuit. Overall, our study provides (1) a resource of candidate CMK-1 targets for further dissecting CaM kinase signaling and (2) evidence of a previously unrecognized, circuit-level antagonism between CMK-1 and calcineurin pathways. These findings highlight a complex interplay of signaling modules that modulate thermal nociception and adaptation, offering new insights into potentially conserved mechanisms that shape nociceptive plasticity and pain (de)sensitization in more complex nervous systems.https://elifesciences.org/articles/103497behavioral plasticitypainkinase substratesCaM kinasecalcineurin
spellingShingle Martina Rudgalvyte
Zehan Hu
Dieter Kressler
Jörn Dengjel
Dominique A Glauser
Antagonist actions of CMK-1/CaMKI and TAX-6/calcineurin along the C. elegans thermal avoidance circuit orchestrate adaptation of nociceptive response to repeated stimuli
eLife
behavioral plasticity
pain
kinase substrates
CaM kinase
calcineurin
title Antagonist actions of CMK-1/CaMKI and TAX-6/calcineurin along the C. elegans thermal avoidance circuit orchestrate adaptation of nociceptive response to repeated stimuli
title_full Antagonist actions of CMK-1/CaMKI and TAX-6/calcineurin along the C. elegans thermal avoidance circuit orchestrate adaptation of nociceptive response to repeated stimuli
title_fullStr Antagonist actions of CMK-1/CaMKI and TAX-6/calcineurin along the C. elegans thermal avoidance circuit orchestrate adaptation of nociceptive response to repeated stimuli
title_full_unstemmed Antagonist actions of CMK-1/CaMKI and TAX-6/calcineurin along the C. elegans thermal avoidance circuit orchestrate adaptation of nociceptive response to repeated stimuli
title_short Antagonist actions of CMK-1/CaMKI and TAX-6/calcineurin along the C. elegans thermal avoidance circuit orchestrate adaptation of nociceptive response to repeated stimuli
title_sort antagonist actions of cmk 1 camki and tax 6 calcineurin along the c elegans thermal avoidance circuit orchestrate adaptation of nociceptive response to repeated stimuli
topic behavioral plasticity
pain
kinase substrates
CaM kinase
calcineurin
url https://elifesciences.org/articles/103497
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