Abstract
BackgroundThe 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.ResultsHere, 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.ConclusionBy 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.
Highlights
The transcription factor AP1 mediates long-term plasticity in vertebrate and invertebrate central nervous systems
These studies indicate that CREB is dispensable for the activity-dependent modulation of bouton number at the Drosophila larval neuromuscular junction (NMJ) [6], a process that shares compelling mechanistic similarities to morphological changes required for long-term facilitation in Aplysia
To confirm and document the expression pattern of this enhancer, we visualized cells in the Drosophila CNS labelled by C380 driven nuclear green fluorescent protein (NlsGFP)
Summary
The transcription factor AP1 mediates long-term plasticity in vertebrate and invertebrate central nervous systems. The generality of the CREB-switch model has been questioned by two previous studies at the Drosophila motor synapse These studies indicate that CREB is dispensable for the activity-dependent modulation of bouton number at the Drosophila larval NMJ [6], a process that shares compelling mechanistic similarities to morphological changes required for long-term facilitation in Aplysia. A recent study suggests that this transcription factor may be AP1 [8], a transcription factor previously shown to be CREB responsive [9,10,11], essential for some forms of long-term memory [12,13], and for long-term cocaine sensitization [14] This recent analysis shows that AP1 activity in the Drosophila CNS, under regulation by endogenous JNK signalling, regulates both bouton number and synaptic strength at the larval motor synapse. Increased levels of CREB mRNA detected in heads of Drosophila after a brief induction of AP1, suggested that AP1 may act upstream of CREB and that AP1 activation may be sufficient to induced CREB dependent and CREB-independent aspects of plasticity [8]
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