| First Author | Blumstein J | Year | 2001 |
| Journal | J Neurosci | Volume | 21 |
| Issue | 20 | Pages | 8034-42 |
| PubMed ID | 11588176 | Mgi Jnum | J:263477 |
| Mgi Id | MGI:6189637 | Doi | 10.1523/JNEUROSCI.21-20-08034.2001 |
| Citation | Blumstein J, et al. (2001) The neuronal form of adaptor protein-3 is required for synaptic vesicle formation from endosomes. J Neurosci 21(20):8034-42 |
| abstractText | Heterotetrameric adaptor complexes vesiculate donor membranes. One of the adaptor protein complexes, AP-3, is present in two forms; one form is expressed in all tissues of the body, whereas the other is restricted to brain. Mice lacking both the ubiquitous and neuronal forms of AP-3 exhibit neurological disorders that are not observed in mice that are mutant only in the ubiquitous form. To begin to understand the role of neuronal AP-3 in neurological disease, we investigated its function in in vitro assays as well as its localization in neural tissue. In the presence of GTPgammaS both ubiquitous and neuronal forms of AP-3 can bind to purified synaptic vesicles. However, only the neuronal form of AP-3 can produce synaptic vesicles from endosomes in vitro. We also identified that the expression of neuronal AP-3 is limited to varicosities of neuronal-like processes and is expressed in most axons of the brain. Although the AP-2/clathrin pathway is the major route of vesicle production and the relatively minor neuronal AP-3 pathway is not necessary for viability, the absence of the latter could lead to the neurological abnormalities seen in mice lacking the expression of AP-3 in brain. In this study we have identified the first brain-specific function for a neuronal adaptor complex. |
