Synaptic and genomic responses to JNK and AP-1 signaling in Drosophila neurons

Persistent Link:
http://hdl.handle.net/10150/610070
Title:
Synaptic and genomic responses to JNK and AP-1 signaling in Drosophila neurons
Author:
Etter, Paul; Narayanan, Radhakrishnan; Navratilova, Zaneta; Patel, Chirag; Bohmann, Dirk; Jasper, Heinrich; Ramaswami, Mani
Affiliation:
Department of Molecular & Cellular Biology, University of Arizona, Tucson, USA; Department of Brain and Cognitive Sciences, MIT, Cambridge, USA; Department of Biomedical Genetics, University of Rochester, Rochester, USA; ARL Division of Neurobiology, University of Arizona, Tucson, USA
Issue Date:
2005
Publisher:
BioMed Central
Citation:
BMC Neuroscience 2005, 6:39 doi:10.1186/1471-2202-6-39
Journal:
BMC Neuroscience
Rights:
© 2005 Etter et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)
Collection Information:
This item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.
Abstract:
BACKGROUND:The transcription factor AP-1 positively controls synaptic plasticity at the Drosophila neuromuscular junction. Although in motor neurons, JNK has been shown to activate AP-1, a positive regulator of growth and strength at the larval NMJ, the consequences of JNK activation are poorly studied. In addition, the downstream transcriptional targets of JNK and AP-1 signaling in the Drosophila nervous system have yet to be identified. Here, we further investigated the role of JNK signaling at this model synapse employing an activated form of JNK-kinase; and using Serial Analysis of Gene Expression and oligonucleotide microarrays, searched for candidate early targets of JNK or AP-1 dependent transcription in neurons.RESULTS:Temporally-controlled JNK induction in postembryonic motor neurons triggers synaptic growth at the NMJ indicating a role in developmental plasticity rather than synaptogenesis. An unexpected observation that JNK activation also causes a reduction in transmitter release is inconsistent with JNK functioning solely through AP-1 and suggests an additional, yet-unidentified pathway for JNK signaling in motor neurons. SAGE profiling of mRNA expression helps define the neural transcriptome in Drosophila. Though many putative AP-1 and JNK target genes arose from the genomic screens, few were confirmed in subsequent validation experiments. One potentially important neuronal AP-1 target discovered, CG6044, was previously implicated in olfactory associative memory. In addition, 5 mRNAs regulated by RU486, a steroid used to trigger conditional gene expression were identified.CONCLUSION:This study demonstrates a novel role for JNK signaling at the larval neuromuscular junction and provides a quantitative profile of gene transcription in Drosophila neurons. While identifying potential JNK/AP-1 targets it reveals the limitations of genome-wide analyses using complex tissues like the whole brain.
EISSN:
1471-2202
DOI:
10.1186/1471-2202-6-39
Version:
Final published version
Additional Links:
http://www.biomedcentral.com/1471-2202/6/39

Full metadata record

DC FieldValue Language
dc.contributor.authorEtter, Paulen
dc.contributor.authorNarayanan, Radhakrishnanen
dc.contributor.authorNavratilova, Zanetaen
dc.contributor.authorPatel, Chiragen
dc.contributor.authorBohmann, Dirken
dc.contributor.authorJasper, Heinrichen
dc.contributor.authorRamaswami, Manien
dc.date.accessioned2016-05-20T08:57:53Z-
dc.date.available2016-05-20T08:57:53Z-
dc.date.issued2005en
dc.identifier.citationBMC Neuroscience 2005, 6:39 doi:10.1186/1471-2202-6-39en
dc.identifier.doi10.1186/1471-2202-6-39en
dc.identifier.urihttp://hdl.handle.net/10150/610070-
dc.description.abstractBACKGROUND:The transcription factor AP-1 positively controls synaptic plasticity at the Drosophila neuromuscular junction. Although in motor neurons, JNK has been shown to activate AP-1, a positive regulator of growth and strength at the larval NMJ, the consequences of JNK activation are poorly studied. In addition, the downstream transcriptional targets of JNK and AP-1 signaling in the Drosophila nervous system have yet to be identified. Here, we further investigated the role of JNK signaling at this model synapse employing an activated form of JNK-kinaseen
dc.description.abstractand using Serial Analysis of Gene Expression and oligonucleotide microarrays, searched for candidate early targets of JNK or AP-1 dependent transcription in neurons.RESULTS:Temporally-controlled JNK induction in postembryonic motor neurons triggers synaptic growth at the NMJ indicating a role in developmental plasticity rather than synaptogenesis. An unexpected observation that JNK activation also causes a reduction in transmitter release is inconsistent with JNK functioning solely through AP-1 and suggests an additional, yet-unidentified pathway for JNK signaling in motor neurons. SAGE profiling of mRNA expression helps define the neural transcriptome in Drosophila. Though many putative AP-1 and JNK target genes arose from the genomic screens, few were confirmed in subsequent validation experiments. One potentially important neuronal AP-1 target discovered, CG6044, was previously implicated in olfactory associative memory. In addition, 5 mRNAs regulated by RU486, a steroid used to trigger conditional gene expression were identified.CONCLUSION:This study demonstrates a novel role for JNK signaling at the larval neuromuscular junction and provides a quantitative profile of gene transcription in Drosophila neurons. While identifying potential JNK/AP-1 targets it reveals the limitations of genome-wide analyses using complex tissues like the whole brain.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttp://www.biomedcentral.com/1471-2202/6/39en
dc.rights© 2005 Etter et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0)en
dc.titleSynaptic and genomic responses to JNK and AP-1 signaling in Drosophila neuronsen
dc.typeArticleen
dc.identifier.eissn1471-2202en
dc.contributor.departmentDepartment of Molecular & Cellular Biology, University of Arizona, Tucson, USAen
dc.contributor.departmentDepartment of Brain and Cognitive Sciences, MIT, Cambridge, USAen
dc.contributor.departmentDepartment of Biomedical Genetics, University of Rochester, Rochester, USAen
dc.contributor.departmentARL Division of Neurobiology, University of Arizona, Tucson, USAen
dc.identifier.journalBMC Neuroscienceen
dc.description.collectioninformationThis item is part of the UA Faculty Publications collection. For more information this item or other items in the UA Campus Repository, contact the University of Arizona Libraries at repository@u.library.arizona.edu.en
dc.eprint.versionFinal published versionen
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