ArticleThe Journal of biological chemistry2005
Domains, amino acid residues, and new isoforms of Caenorhabditis elegans diacylglycerol kinase 1 (DGK-1) important for terminating diacylglycerol signaling in vivo.
Article in The Journal of biological chemistry, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 35 citations in OpenAlex.
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- Selecting genes for analysis using historically contingent progress: from RNA changes to protein-protein interactions.bioRxiv : the preprint server for biology · 2024Article
- The Bacterial GJournal of chemical ecology · 2023Article
- Regulation of Diacylglycerol Content in Olfactory Neurons Determines Forgetting or Retrieval of Olfactory Memory inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
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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
- Phospholipase D functional ablation has a protective effect in an Alzheimer's disease Caenorhabditis elegans model.Scientific reports · 2018Article
- Function of alternative splicing.Gene · 2013Review
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- Serotonin activates overall feeding by activating two separate neural pathways in Caenorhabditis elegans.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Regulation of serotonin biosynthesis by the G proteins Galphao and Galphaq controls serotonin signaling in Caenorhabditis elegans.Genetics · 2008Article
- Trio's Rho-specific GEF domain is the missing Galpha q effector in C. elegans.Genes & development · 2007Article
- Presynaptic Ca2+/calmodulin-dependent protein kinase II modulates neurotransmitter release by activating BK channels at Caenorhabditis elegans neuromuscular junction.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2007Article
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- Goalpha regulates olfactory adaptation by antagonizing Gqalpha-DAG signaling in Caenorhabditis elegans.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Rho is a presynaptic activator of neurotransmitter release at pre-existing synapses in C. elegans.Genes & development · 2006Article
- Diacylglycerol kinases in membrane trafficking.Cellular logisticsReview
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Diacylglycerol kinases (DGKs) inhibit diacylglycerol (DAG) signaling by phosphorylating DAG. DGK-1, the Caenorhabditis elegans ortholog of human neuronal DGK, inhibits neurotransmission to control behavior. DGK-1, like DGK, has three cysteine-rich domains (CRDs), a pleckstrin homology domain, and a kinase domain. To identify DGK domains and amino acid residues critical for terminating DAG signaling in vivo, we analyzed 20 dgk-1 mutants defective in DGK-1-controlled behaviors. We found by sequencing that the mutations included nine amino acid substitutions and seven premature stop codons that impair the physiological functions of DGK-1. All nine amino acid substitutions are in the second CRD, the third CRD, or the kinase domain. Thus, these domains are important for the termination of DAG signaling by DGK-1 in vivo. Seven of the substituted amino acid residues are present in all human DGKs and likely define key residues required for the function of all DGKs. An ATP-binding site mutation expected to inactivate the kinase domain retained very little physiological function, but we found two stop codon mutants predicted to truncate DGK-1 before its kinase domain that retained significantly more function. We detected novel splice forms of dgk-1 that can reconcile this apparent conflict, as they skip exons containing the stop codons to produce DGK-1 isoforms that contain the kinase domain. Two of these isoforms lack an intact pleckstrin homology domain and yet appear to have significant function. Additional novel isoform(s) account for all of the DGK-1 function necessary for one behavior, dopamine response.
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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.