Evidence for cell autonomous AP1 function in regulation of Drosophila motor-neuron plasticity

Persistent Link:
http://hdl.handle.net/10150/610069
Title:
Evidence for cell autonomous AP1 function in regulation of Drosophila motor-neuron plasticity
Author:
Sanyal, Subhabrata; Narayanan, Radhakrishnan; Consoulas, Christos; Ramaswami, Mani
Affiliation:
Department of Molecular & Cellular Biology, Box 210106 University of Arizona, 1007 E. Lowell Street, Tucson AZ 85721, USA; Department of Experimental Physiology, Medical School, University of Athens, Athens, Greece; ARL Division of Neurobiology, University of Arizona, Tucson AZ 85721, USA
Issue Date:
2003
Publisher:
BioMed Central
Citation:
BMC Neuroscience 2003, 4:20 http://www.biomedcentral.com/1471-2202/4/20
Journal:
BMC Neuroscience
Rights:
© 2003 Sanyal et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.
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 AP1 mediates long-term plasticity in vertebrate and invertebrate central nervous systems. Recent studies of activity-induced synaptic change indicate that AP1 can function upstream of CREB to regulate both CREB-dependent enhancement of synaptic strength as well as CREB-independent increase in bouton number at the Drosophila neuromuscular junction (NMJ). However, it is not clear from this study if AP1 functions autonomously in motor neurons to directly modulate plasticity.RESULTS:Here, we show that Fos and Jun, the two components of AP1, are abundantly expressed in motor neurons. We further combine immunohistochemical and electrophysiological analyses with use of a collection of enhancers that tightly restrict AP1 transgene expression within the nervous system to show that AP1 induction or inhibition in, but not outside of, motor neurons is necessary and sufficient for its modulation of NMJ size and strength.CONCLUSION:By arguing against the possibility that AP1 effects at the NMJ occur via a polysynaptic mechanism, these observations support a model in which AP1 directly modulates NMJ plasticity processes through a cell autonomous pathway in the motor neuron. The approach described here may serve as a useful experimental paradigm for analyzing cell autonomy of genes found to influence structure and function of Drosophila motor neurons.
EISSN:
1471-2202
DOI:
10.1186/1471-2202-4-20
Version:
Final published version
Additional Links:
http://www.biomedcentral.com/1471-2202/4/20

Full metadata record

DC FieldValue Language
dc.contributor.authorSanyal, Subhabrataen
dc.contributor.authorNarayanan, Radhakrishnanen
dc.contributor.authorConsoulas, Christosen
dc.contributor.authorRamaswami, Manien
dc.date.accessioned2016-05-20T08:57:52Z-
dc.date.available2016-05-20T08:57:52Z-
dc.date.issued2003en
dc.identifier.citationBMC Neuroscience 2003, 4:20 http://www.biomedcentral.com/1471-2202/4/20en
dc.identifier.doi10.1186/1471-2202-4-20en
dc.identifier.urihttp://hdl.handle.net/10150/610069-
dc.description.abstractBACKGROUND:The transcription factor AP1 mediates long-term plasticity in vertebrate and invertebrate central nervous systems. Recent studies of activity-induced synaptic change indicate that AP1 can function upstream of CREB to regulate both CREB-dependent enhancement of synaptic strength as well as CREB-independent increase in bouton number at the Drosophila neuromuscular junction (NMJ). However, it is not clear from this study if AP1 functions autonomously in motor neurons to directly modulate plasticity.RESULTS:Here, we show that Fos and Jun, the two components of AP1, are abundantly expressed in motor neurons. We further combine immunohistochemical and electrophysiological analyses with use of a collection of enhancers that tightly restrict AP1 transgene expression within the nervous system to show that AP1 induction or inhibition in, but not outside of, motor neurons is necessary and sufficient for its modulation of NMJ size and strength.CONCLUSION:By arguing against the possibility that AP1 effects at the NMJ occur via a polysynaptic mechanism, these observations support a model in which AP1 directly modulates NMJ plasticity processes through a cell autonomous pathway in the motor neuron. The approach described here may serve as a useful experimental paradigm for analyzing cell autonomy of genes found to influence structure and function of Drosophila motor neurons.en
dc.language.isoenen
dc.publisherBioMed Centralen
dc.relation.urlhttp://www.biomedcentral.com/1471-2202/4/20en
dc.rights© 2003 Sanyal et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.en
dc.titleEvidence for cell autonomous AP1 function in regulation of Drosophila motor-neuron plasticityen
dc.typeArticleen
dc.identifier.eissn1471-2202en
dc.contributor.departmentDepartment of Molecular & Cellular Biology, Box 210106 University of Arizona, 1007 E. Lowell Street, Tucson AZ 85721, USAen
dc.contributor.departmentDepartment of Experimental Physiology, Medical School, University of Athens, Athens, Greeceen
dc.contributor.departmentARL Division of Neurobiology, University of Arizona, Tucson AZ 85721, 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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