@article {46425,
	title = {Glial-derived prodegenerative signaling in the Drosophila neuromuscular system.},
	journal = {Neuron},
	volume = {72},
	year = {2011},
	month = {2011 Dec 8},
	pages = {760-75},
	abstract = {<p>We provide evidence for a prodegenerative, glial-derived signaling framework in the Drosophila neuromuscular system that includes caspase and mitochondria-dependent signaling. We demonstrate that Drosophila TNF-α (eiger) is expressed in a subset of peripheral glia, and the TNF-α receptor (TNFR), Wengen, is expressed in motoneurons. NMJ degeneration caused by disruption of the spectrin/ankyrin skeleton is suppressed by an eiger mutation or by eiger knockdown within a subset of peripheral glia. Loss of wengen in motoneurons causes a similar suppression providing evidence for glial-derived prodegenerative TNF-α signaling. Neither JNK nor NFκβ is required for prodegenerative signaling. However, we provide evidence for the involvement of both an initiator and effector caspase, Dronc and Dcp-1, and mitochondrial-dependent signaling. Mutations that deplete the axon and nerve terminal of mitochondria suppress degeneration as do mutations in Drosophila Bcl-2 (debcl), a mitochondria-associated protein, and Apaf-1 (dark), which links mitochondrial signaling with caspase activity in other systems.</p>
},
	keywords = {Animals, Animals, Genetically Modified, Apoptotic Protease-Activating Factor 1, Caspases, Disease Models, Animal, Drosophila, Drosophila Proteins, Excitatory Postsynaptic Potentials, Fluorescence Recovery After Photobleaching, Green Fluorescent Proteins, Mitochondria, Motor Neuron Disease, Mutation, Nerve Degeneration, Nerve Tissue Proteins, Neuroglia, Neuromuscular Junction, Proto-Oncogene Proteins, Receptors, Tumor Necrosis Factor, RNA Interference, Signal Transduction},
	issn = {1097-4199},
	doi = {10.1016/j.neuron.2011.09.031},
	author = {Keller, Lani C and Cheng, Ling and Locke, Cody J and M{\"u}ller, Martin and Fetter, Richard D and Davis, Graeme W}
}
