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http://purl.uniprot.org/citations/15932641http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/15932641http://www.w3.org/2000/01/rdf-schema#comment"

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."xsd:string
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http://purl.uniprot.org/citations/15932641http://purl.uniprot.org/core/author"Bohmann D."xsd:string
http://purl.uniprot.org/citations/15932641http://purl.uniprot.org/core/author"Patel C."xsd:string
http://purl.uniprot.org/citations/15932641http://purl.uniprot.org/core/author"Ramaswami M."xsd:string
http://purl.uniprot.org/citations/15932641http://purl.uniprot.org/core/author"Narayanan R."xsd:string
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http://purl.uniprot.org/citations/15932641http://purl.uniprot.org/core/author"Etter P.D."xsd:string
http://purl.uniprot.org/citations/15932641http://purl.uniprot.org/core/author"Navratilova Z."xsd:string
http://purl.uniprot.org/citations/15932641http://purl.uniprot.org/core/date"2005"xsd:gYear
http://purl.uniprot.org/citations/15932641http://purl.uniprot.org/core/name"BMC Neurosci"xsd:string
http://purl.uniprot.org/citations/15932641http://purl.uniprot.org/core/pages"39"xsd:string
http://purl.uniprot.org/citations/15932641http://purl.uniprot.org/core/title"Synaptic and genomic responses to JNK and AP-1 signaling in Drosophila neurons."xsd:string
http://purl.uniprot.org/citations/15932641http://purl.uniprot.org/core/volume"6"xsd:string
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