Document Detail


Temporal coherency between receptor expression, neural activity and AP-1-dependent transcription regulates Drosophila motoneuron dendrite development.
MedLine Citation:
PMID:  23293292     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Neural activity has profound effects on the development of dendritic structure. Mechanisms that link neural activity to nuclear gene expression include activity-regulated factors, such as CREB, Crest or Mef2, as well as activity-regulated immediate-early genes, such as fos and jun. This study investigates the role of the transcriptional regulator AP-1, a Fos-Jun heterodimer, in activity-dependent dendritic structure development. We combine genetic manipulation, imaging and quantitative dendritic architecture analysis in a Drosophila single neuron model, the individually identified motoneuron MN5. First, Dα7 nicotinic acetylcholine receptors (nAChRs) and AP-1 are required for normal MN5 dendritic growth. Second, AP-1 functions downstream of activity during MN5 dendritic growth. Third, using a newly engineered AP-1 reporter we demonstrate that AP-1 transcriptional activity is downstream of Dα7 nAChRs and Calcium/calmodulin-dependent protein kinase II (CaMKII) signaling. Fourth, AP-1 can have opposite effects on dendritic development, depending on the timing of activation. Enhancing excitability or AP-1 activity after MN5 cholinergic synapses and primary dendrites have formed causes dendritic branching, whereas premature AP-1 expression or induced activity prior to excitatory synapse formation disrupts dendritic growth. Finally, AP-1 transcriptional activity and dendritic growth are affected by MN5 firing only during development but not in the adult. Our results highlight the importance of timing in the growth and plasticity of neuronal dendrites by defining a developmental period of activity-dependent AP-1 induction that is temporally locked to cholinergic synapse formation and dendritic refinement, thus significantly refining prior models derived from chronic expression studies.
Authors:
Fernando Vonhoff; Claudia Kuehn; Sonja Blumenstock; Subhabrata Sanyal; Carsten Duch
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural    
Journal Detail:
Title:  Development (Cambridge, England)     Volume:  140     ISSN:  1477-9129     ISO Abbreviation:  Development     Publication Date:  2013 Feb 
Date Detail:
Created Date:  2013-01-07     Completed Date:  2013-03-07     Revised Date:  2014-02-04    
Medline Journal Info:
Nlm Unique ID:  8701744     Medline TA:  Development     Country:  England    
Other Details:
Languages:  eng     Pagination:  606-16     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Genetically Modified
Calcium-Calmodulin-Dependent Protein Kinase Type 2 / genetics,  metabolism
Cell Nucleus / genetics,  metabolism
Cholinergic Neurons / metabolism
Dendrites / genetics,  metabolism*
Drosophila Proteins / genetics,  metabolism
Drosophila melanogaster / embryology,  genetics,  metabolism*
Embryo, Nonmammalian / cytology,  embryology,  metabolism
Enzyme Activation
Gene Expression Regulation, Developmental*
Genes, Reporter
Immunohistochemistry / methods
Microscopy, Confocal / methods
Microscopy, Fluorescence
Receptors, Nicotinic / genetics,  metabolism
Signal Transduction
Synaptic Transmission
Time Factors
Transcription Factor AP-1 / genetics,  metabolism*
Transcription, Genetic*
Transcriptional Activation
Grant Support
ID/Acronym/Agency:
5R21MH091520/MH/NIMH NIH HHS; R01 NS072128/NS/NINDS NIH HHS; R01NS072128/NS/NINDS NIH HHS; S10RR027154/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Drosophila Proteins; 0/Receptors, Nicotinic; 0/Transcription Factor AP-1; 0/kayak protein, Drosophila; 0/nicotinic acetylcholine receptor alpha-subunits, Drosophila; EC 2.7.11.17/Calcium-Calmodulin-Dependent Protein Kinase Type 2
Comments/Corrections

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