G protein coupled receptor kinases modulate Caenorhabditis elegans reactions to heat stresses

Heilman, Christian; Ibarreta, Janeen; Salonga, Glecille Ann; Hon, Michelle; Caracci, Angela M.; Badial, Tajinder; Crivello, Selina; Henry, Stacy A.; Nguyen, Tina M.; So, Christopher H.

doi:10.1016/j.bbrc.2020.07.121

Cited by 6 publications

(4 citation statements)

References 24 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…elegans , which lacks a visual system, has GRK-1 and GRK-2, which are orthologs of the mammalian GRK4/5/6 and GRK2/3 families, respectively [ 23 , 24 ]. grk-2 is expressed broadly in the nervous system and has a broad impact on animal physiology including chemosensation [ 23 ], gustatory plasticity [ 25 ], egg-laying [ 26 ], crawling [ 27 ], swimming [ 27 , 28 ], and oxidative and heat stress responses [ 29 , 30 ]. Elimination of grk-2 function renders animals unable to respond to a wide range of chemical stimuli, suggesting that GRK-2 plays a positive role in chemosensation [ 23 ].…”

Section: Introductionmentioning

confidence: 99%

G protein-coupled receptor kinase-2 (GRK-2) controls exploration through neuropeptide signaling in Caenorhabditis elegans

et al. 2023

View full text Add to dashboard Cite

Animals alter their behavior in manners that depend on environmental conditions as well as their developmental and metabolic states. For example, C. elegans is quiescent during larval molts or during conditions of satiety. By contrast, worms enter an exploration state when removed from food. Sensory perception influences movement quiescence (defined as a lack of body movement), as well as the expression of additional locomotor states in C. elegans that are associated with increased or reduced locomotion activity, such as roaming (exploration behavior) and dwelling (local search). Here we find that movement quiescence is enhanced, and exploration behavior is reduced in G protein-coupled receptor kinase grk-2 mutant animals. grk-2 was previously shown to act in chemosensation, locomotion, and egg-laying behaviors. Using neuron-specific rescuing experiments, we show that GRK-2 acts in multiple ciliated chemosensory neurons to control exploration behavior. grk-2 acts in opposite ways from the cGMP-dependent protein kinase gene egl-4 to control movement quiescence and exploration behavior. Analysis of mutants with defects in ciliated sensory neurons indicates that grk-2 and the cilium-structure mutants act in the same pathway to control exploration behavior. We find that GRK-2 controls exploration behavior in an opposite manner from the neuropeptide receptor NPR-1 and the neuropeptides FLP-1 and FLP-18. Finally, we show that secretion of the FLP-1 neuropeptide is negatively regulated by GRK-2 and that overexpression of FLP-1 reduces exploration behavior. These results define neurons and molecular pathways that modulate movement quiescence and exploration behavior.

show abstract

Section: Introductionmentioning

confidence: 99%

G protein-coupled receptor kinase-2 (GRK-2) controls exploration through neuropeptide signaling in Caenorhabditis elegans

et al. 2023

View full text Add to dashboard Cite

show abstract

Section: Resultsmentioning

confidence: 99%

Multiple p38/JNK mitogen-activated protein kinase (MAPK) signaling pathways mediate salt chemotaxis learning in C. elegans

Huang

Suzuki

Kunitomo

et al. 2023

G3: Genes, Genomes, Genetics

View full text Add to dashboard Cite

Animals are able to adapt their behaviors to their environment. In order to achieve this, the nervous system plays integrative roles, such as perception of external signals, sensory processing, and behavioral regulations via various signal transduction pathways. Here genetic analyses of C. elegans found that mutants of components of JNK and p38 Mitogen-activated protein kinase (MAPK) signaling pathways, also known as stress-activated protein kinase (SAPK) signaling pathways, exhibit various types of defects in the learning of salt chemotaxis. C. elegans homologues of JNK MAPKKK and MAPKK, MLK-1 and MEK-1, respectively, are required to avoid salt concentrations experienced during starvation. In contrast, homologues of p38 MAPKKK and MAPKK, NSY-1 and SEK-1, respectively, are required for high-salt chemotaxis after conditioning. Genetic interaction analyses suggest that a JNK family MAPK, KGB-1, functions downstream of both signaling pathways to regulate salt chemotaxis learning. Furthermore, we found that the NSY-1/SEK-1 pathway functions in sensory neurons, ASH, ADF, and ASER, to regulate the learned high-salt chemotaxis. A neuropeptide, NLP-3, expressed in ASH, ADF, and ASER neurons, and a neuropeptide receptor, NPR-15, expressed in AIA interneurons that receive synaptic input from these sensory neurons, function in the same genetic pathway as NSY-1/SEK-1 signaling. These findings suggest that this MAPK pathway may affect neuropeptide signaling between sensory neurons and interneurons, thus promoting high-salt chemotaxis after conditioning.

show abstract

“…In C. elegans, there are two GRK homologs, GRK-1 and GRK-2. The C. elegans ortholog of mammalian GRK2/3, GRK-2, but not GRK-1, is involved in SAPK-dependent stress responses, such as oxidative and heat stress (Henry et al, 2021;Heilman et al, 2020). These previous reports implied that GRK-2 may modulate SAPKs in C. elegans and be involved in salt chemotaxis learning regulation.…”

Section: Grk-2 Functions In the Sek-1 Pathway In Salt Chemotaxis Lear...mentioning

confidence: 99%

Multiple p38/JNK Mitogen-activated protein kinase (MAPK) signaling pathways mediate salt chemotaxis learning inC. elegans

Huang

Suzuki

Kunitomo

et al. 2023

Preprint

View full text Add to dashboard Cite

Animals are able to adapt their behaviors to their environment. In order to achieve this, the nervous system plays integrative roles, such as perception of external signals, sensory processing, and behavioral regulations via various signal transduction pathways. Here genetic analyses ofC. elegansfound that mutants of components of JNK and p38 Mitogen-activated protein kinase (MAPK) signaling pathways, also known as stress-activated protein kinase (SAPK) signaling pathways, exhibit various types of defects in the learning of salt chemotaxis.C. eleganshomologues of JNK MAPKKK and MAPKK, MLK-1 and MEK-1, respectively, are required to avoid salt concentrations experienced during starvation. In contrast, homologues of p38 MAPKKK and MAPKK, NSY-1 and SEK-1, respectively, are required for high-salt chemotaxis after conditioning. Genetic interaction analyses suggest that a JNK family MAPK, KGB-1, functions downstream of both signaling pathways to regulate salt chemotaxis learning. Furthermore, we found that the NSY-1/SEK-1 pathway functions in sensory neurons, ASH, ADF, and ASER, to regulate the learned high-salt chemotaxis. A neuropeptide, NLP-3, expressed in ASH, ADF, and ASER neurons, and a neuropeptide receptor, NPR-15, expressed in AIA interneurons that receive synaptic input from these sensory neurons, function in the same genetic pathway as NSY-1 / SEK-1 signaling. These findings suggest that this MAPK pathway may affect neuropeptide signaling between sensory neurons and interneurons, thus promoting high-salt chemotaxis after conditioning.

show abstract

G protein coupled receptor kinases modulate Caenorhabditis elegans reactions to heat stresses

Cited by 6 publications

References 24 publications

G protein-coupled receptor kinase-2 (GRK-2) controls exploration through neuropeptide signaling in Caenorhabditis elegans

G protein-coupled receptor kinase-2 (GRK-2) controls exploration through neuropeptide signaling in Caenorhabditis elegans

Multiple p38/JNK mitogen-activated protein kinase (MAPK) signaling pathways mediate salt chemotaxis learning in C. elegans

Multiple p38/JNK Mitogen-activated protein kinase (MAPK) signaling pathways mediate salt chemotaxis learning inC. elegans

Contact Info

Product

Resources

About