NF-κB, IκB, and IRAK control glutamate receptor density at the Drosophila NMJ.

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Neuron. 2007 Sep 20;55(6):859-73. doi: 10.1016/j.neuron.2007.08.005

NF-κB, IκB, and IRAK control glutamate receptor density at the Drosophila NMJ. Fetter LabSimpson Lab

Heckscher ES, Fetter RD, Marek KW, Albin SD, Davis GW

Note: Research in this publication was not performed at Janelia.

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Abstract

NF-κB signaling has been implicated in neurodegenerative disease, epilepsy, and neuronal plasticity. However, the cellular and molecular activity of NF-κB signaling within the nervous system remains to be clearly defined. Here, we show that the NF-κB and IκB homologs Dorsal and Cactus surround postsynaptic glutamate receptor (GluR) clusters at the Drosophila NMJ. We then show that mutations in dorsal, cactus, and IRAK/pelle kinase specifically impair GluR levels, assayed immunohistochemically and electrophysiologically, without affecting NMJ growth, the size of the postsynaptic density, or homeostatic plasticity. Additional genetic experiments support the conclusion that cactus functions in concert with, rather than in opposition to, dorsal and pelle in this process. Finally, we provide evidence that Dorsal and Cactus act posttranscriptionally, outside the nucleus, to control GluR density. Based upon our data we speculate that Dorsal, Cactus, and Pelle could function together, locally at the postsynaptic density, to specify GluR levels.

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NF-κB, IκB, and IRAK control glutamate receptor density at the Drosophila NMJ.

Note: Research in this publication was not performed at Janelia.

Abstract

Janelia Authors