title: Evidence for cell autonomous AP1 function in regulation of Drosophila motor-neuron plasticity.
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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Molecular & Cellular Biology, Box 210106 University of Arizona, 1007 E, Lowell Street, Tucson AZ 85721, USA. sanyal@u.arizona.edu
authors.forename: Subhabrata
authors.initials: S
authors.lastname: Sanyal
authors.forename: Radhakrishnan
authors.initials: R
authors.lastname: Narayanan
authors.forename: Christos
authors.initials: C
authors.lastname: Consoulas
authors.forename: Mani
authors.initials: M
authors.lastname: Ramaswami
mesh_terms: D000818:Animals; D000943:Antigens, Differentiation / Q000096:biosynthesis; D002799:Cholinergic Fibers / Q000378:metabolism; D004330:Drosophila / Q000502:physiology*; D029721:Drosophila Proteins / Q000378:metabolism; D005071:Evoked Potentials / Q000502:physiology; D005260:Female; D005786:Gene Expression Regulation / Q000502:physiology*; D049452:Green Fluorescent Proteins; D007814:Larva; D008164:Luminescent Proteins / Q000096:biosynthesis / Q000235:genetics; D008297:Male; D008959:Models, Neurological; D009046:Motor Neurons / Q000378:metabolism / Q000502:physiology*; D009132:Muscles / Q000378:metabolism; D009469:Neuromuscular Junction / Q000502:physiology; D009473:Neuronal Plasticity / Q000502:physiology*; D016755:Proto-Oncogene Proteins c-jun / Q000378:metabolism; D018808:Transcription Factor AP-1 / Q000235:genetics / Q000378:metabolism*; D019076:Transgenes
chemical_list: D000943:Antigens, Differentiation; D029721:Drosophila Proteins; D008164:Luminescent Proteins; D016755:Proto-Oncogene Proteins c-jun; D018808:Transcription Factor AP-1; C435749:kay protein, Drosophila; D049452:Green Fluorescent Proteins