Synaptic and genomic responses to JNK and AP-1 signaling in Drosophilaneurons
Name
1471-2202-6-39.pdf
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1.75 MB
Format
Adobe PDF
Checksum (MD5)
48382b9eac71015aa135dd8bd12f014f
Author(s)
Narayanan, Radhakrishnan
Navratilova, Zaneta
Patel, Chirag
Bohmann, Dirk
Ramaswami, Mani
Jasper, Heinrich
Etter, Paul D.
Date Issued
June 2005
Journal
BMC Neuroscience
Publisher
BioMed Central Ltd
Citation
BMC Neuroscience. 2005 Jun 02;6(1):39
Version
Final published version
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.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
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Creative Commons Attribution
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DOI of Published Version
https://doi.org/10.1186/1471-2202-6-39
