ArticleProceedings of the National Academy of Sciences of the United States of America2006
Goalpha regulates olfactory adaptation by antagonizing Gqalpha-DAG signaling in Caenorhabditis elegans.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 88 citations in OpenAlex.
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- BRCA1-BARD1 Regulates Axon Regeneration in Concert with the Gqα-DAG Signaling Network.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Chemosensory signal transduction in Caenorhabditis elegans.Genetics · 2021Review
- Sex-specific regulation of neuronal functions in Caenorhabditis elegans: the sex-determining protein TRA-1 represses goa-1/GαMolecular genetics and genomics : MGG · 2020Article
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- Neurotransmitter signaling through heterotrimeric G proteins: insights from studies in C. elegans.WormBook : the online review of C. elegans biology · 2018Review
- Loss of CaMKI Function Disrupts Salt Aversive Learning inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- [Molecular and cell biological mechanism of olfactory adaptation inZhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2018Review
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3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The heterotrimeric G protein G(o) is abundantly expressed in the mammalian nervous system and modulates neural activities in response to various ligands. However, G(o)'s functions in living animals are less well understood. Here, we demonstrate that GOA-1 G(o)alpha has a fundamental role in olfactory adaptation in Caenorhabditis elegans. Impairment of GOA-1 G(o)alpha function and excessive activation of EGL-30 G(q)alpha cause a defect in adaptation to AWC-sensed odorants. These pathways antagonistically modulate olfactory adaptation in AWC chemosensory neurons. Wild-type animals treated with phorbol esters and double-mutant animals of diacylglycerol (DAG) kinases, dgk-3; dgk-1, also have a defect in adaptation, suggesting that elevated DAG signals disrupt normal adaptation. Constitutively active GOA-1 can suppress the adaptation defect of dgk-3; dgk-1 double mutants, whereas it fails to suppress the adaptation defect of animals with constitutively active EGL-30, implying that GOA-1 acts upstream of EGL-30 in olfactory adaptation. Our results suggest that down-regulation of EGL-30-DAG signaling by GOA-1 underlies olfactory adaptation and plasticity of chemotaxis.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.