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Published online
doi:10.1083/jcb.200903166
The Journal of Cell Biology, Vol. 187, No. 1, 101-117
The Rockefeller University Press, 0021-9525 $30.00
© Massaro et al.
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Article

Molecular mechanisms that enhance synapse stability despite persistent disruption of the spectrin/ankyrin/microtubule cytoskeleton



Catherine M. Massaro, Jan Pielage, and Graeme W. Davis

Department of Biochemistry and Biophysics, Program in Neuroscience, University of California, San Francisco, San Francisco, CA 94158

Correspondence to Graeme W. Davis: gdavis{at}biochem.ucsf.edu

Loss of spectrin or ankyrin in the presynaptic motoneuron disrupts the synaptic microtubule cytoskeleton and leads to disassembly of the neuromuscular junction (NMJ). Here, we demonstrate that NMJ disassembly after loss of {alpha}-spectrin can be suppressed by expression of a WldS transgene, providing evidence for a Wallerian-type degenerative mechanism. We then identify a second signaling system. Enhanced MAPK-JNK-Fos signaling suppresses NMJ disassembly despite loss of presynaptic {alpha}-spectrin or ankyrin2-L. This signaling system is activated after an acute cytoskeletal disruption, suggesting an endogenous role during neurological stress. This signaling system also includes delayed, negative feedback via the JNK phosphatase puckered, which inhibits JNK-Fos to allow NMJ disassembly in the presence of persistent cytoskeletal stress. Finally, the MAPK-JNK pathway is not required for baseline NMJ stabilization during normal NMJ growth. We present a model in which signaling via JNK-Fos functions as a stress response system that is transiently activated after cytoskeletal disruption to enhance NMJ stability, and is then shut off allowing NMJ disassembly during persistent cytoskeletal disruption.

Abbreviations used in this paper: ALS, amyotrophic lateral sclerosis; BMP, bone morphogenetic protein; MT, microtubule; NMJ, neuromuscular junction.

© 2009 Massaro et al.
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