Cell Survival through Trk Neurotrophin Receptors Is Differentially Regulated by Ubiquitination

Authors:
Arevalo JC, Waite J, Rajagopal R, Beyna M, Chen ZY, Lee FS, Chao MV
In:
Source: Neuron
Publication Date: (2006)
Issue: 50(4): 549-59
Research Area:
Neurobiology
Cells used in publication:
Neuron, hippo/cortical, rat
Species: rat
Tissue Origin: brain
Neuron, mesencephalic, rat
Species: rat
Tissue Origin: brain
Neuron, hippocampal, rat
Species: rat
Tissue Origin: brain
Platform:
Nucleofector® I/II/2b
Abstract
Specificity of neurotrophin factor signaling is dictated through the action of Trk receptor tyrosine kinases. Once activated, Trk receptors are internalized and targeted for degradation. However, the mechanisms implicated in this process are incompletely understood. Here we report that the Trk receptors are multimonoubiquitinated in response to neurotrophins. We have identified an E3 ubiquitin ligase, Nedd4-2, that associates with the TrkA receptor and is phosphorylated upon NGF binding. The binding of Nedd4-2 to TrkA through a PPXY motif leads to the ubiquitination and downregulation of TrkA. Activated TrkA receptor levels and the survival of NGF-dependent sensory neurons, but not BDNF-dependent sensory neurons, are directly influenced by Nedd4-2 expression. Unexpectedly, Nedd4-2 does not bind or ubiquitinate related TrkB receptors, due to the lack of a consensus PPXY motif. Our results indicate that Trk neurotrophin receptors are differentially regulated by ubiquitination to modulate the survival of neurons.