Pi31 Is An Adaptor Protein For Proteasome Transport In Axons And Required For Synaptic Development

Protein degradation by the ubiquitin proteasome system ups is critical for neuronal development plasticity and function.

Pi31 is an adaptor protein for proteasome transport in axons and required for synaptic development. This mechanism is required for protein homeostasis and synaptic architecture. Pi31 is an adaptor protein for proteasome transport in axons and required for synaptic development. Pi31 is an adaptor protein for proteasome transport in axons and required for synaptic development graphical abstract highlights d pi31 directly mediates the formation of dynein light chain proteasome complexes d pi31 is required for axonal transport of proteasomes in drosophila and mice d stress regulates pi31 activity through p38 mapk mediated. Pi31 is an adaptor protein for proteasome transport in axons and required for synaptic development.

Proteasomes are actively transported between the soma and terminals of neurons. Neurons utilize microtubule dependent molecular motors to allocate proteasomes to synapses but how proteasomes are coupled to motor proteins and how this transport is regulated to meet changing demand for protein breakdown remains largely unknown. We generated global and conditional pi31 knockout mouse strains and show that this protein is required for protein homeostasis and that its conditional inactivation in neurons disrupts synaptic. Liu k 1 jones s 1 minis a 1 rodriguez j 1 molina h 2 steller h 3.

Taken together these results show that pi31 is a direct adaptor protein that mediates the formation of a complex between proteasomes and ddynll1 and this activity is enhanced by phosphorylation of pi31. The conserved proteasome binding protein pi31 serves as an adapter to couple proteasomes with cellular motors to mediate their transport to distal tips of neurons where protein breakdown occurs. We show that the conserved proteasome binding protein pi31 serves as an adaptor to couple proteasomes with dynein light chain proteins dynll1 2. The inactivation of pi31 inhibited proteasome motility in axons and disrupted synaptic.

1 strang laboratory of apoptosis and cancer biology the rockefeller university 1230 york avenue new york ny 10065 usa. Show that pi31 couples proteasomes to cellular motors for fast axonal transport and thereby brings proteasomes to sites where protein breakdown occurs. Kai liu et al.