Protein kinase D regulates trafficking of dendritic membrane proteins in developing neurons

Bisbal M.; Conde, C; Donoso M.; Bollati F.; Sesma, J; Quiroga S.; Anel, AD; MALHOTRA V.; Marzolo, MP; Cáceres A.

Abstract

In non-neuronal cells, inactivation of protein kinase D (PKD) blocks fission of trans-Golgi network (TGN) transport carriers, inducing the appearance of long tubules filled with cargo. We now report on the function of PKD1 in neuronal protein trafficking. In cultured hippocampal pyramidal cells, the transferrin receptor (TfR) and the low-density receptor-related protein (LRP) are predominantly transported to dendrites and excluded from axons. Expression of kinase-inactive PKD1 or its depletion by RNA interference treatment dramatically and selectively alter the intracellular trafficking and membrane delivery of TfR- and LRP-containing vesicles, without inhibiting exit from the TGN or inducing Golgi tubulation. After PKD1 suppression, dendritic membrane proteins are mispackaged into carriers that transport VAMP2; these vesicles are distributed to both axons and dendrites, but are rapidly endocytosed from dendrites and preferentially delivered to the axonal membrane. A kinase-defective mutant of PKD1 lacking the ability to bind diacylglycerol and hence its Golgi localization does not cause missorting of TfR or LRP. These results suggest that in neurons PKD1 regulates TGN-derived sorting of dendritic proteins and hence has a role in neuronal polarity. Copyright © 2008 Society for Neuroscience.

Más información

Título según WOS: Protein kinase D regulates trafficking of dendritic membrane proteins in developing neurons
Título según SCOPUS: Protein kinase D regulates trafficking of dendritic membrane proteins in developing neurons
Título de la Revista: JOURNAL OF NEUROSCIENCE
Volumen: 28
Número: 37
Editorial: SOC NEUROSCIENCE
Fecha de publicación: 2008
Página de inicio: 9297
Página final: 9308
Idioma: English
URL: http://www.jneurosci.org/cgi/doi/10.1523/JNEUROSCI.1879-08.2008
DOI:

10.1523/JNEUROSCI.1879-08.2008

Notas: ISI, SCOPUS