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Published 11 April 2005. doi:10.1083/jcb.200412089
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 169, Number 1, 83-91
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Article

 PKC{eta} is required for ß1{gamma}2/ß3{gamma}2- and PKD-mediated transport to the cell surface and the organization of the Golgi apparatus

Alberto Marcelo Díaz Añel and Vivek Malhotra

Department of Biology, University of California, San Diego, La Jolla, CA 92093

Correspondence to Vivek Malhotra: malhotra{at}biomail.ucsd.edu

Protein kinase D (PKD) binds to a pool of diacylglycerol (DAG) in the TGN and undergoes a process of activation that involves heterotrimeric GTP-binding protein subunits ß{gamma} to regulate membrane fission. This fission reaction is used to generate transport carriers at the TGN that are en route to the cell surface. We now report that PKD is activated specifically by G protein subunit ß1{gamma}2 and ß3{gamma}2 via the Golgi apparatus–associated PKC{eta}. Compromising the kinase activity of PKC{eta}-inhibited protein transport from TGN to the cell surface. Expression of constitutively activated PKC{eta} caused Golgi fragmentation, which was inhibited by a kinase inactive form of PKD. Our findings reveal that ß{gamma}, PKC{eta}, and PKD act in series to generate transport carriers from the TGN and their overactivation results in complete vesiculation of the Golgi apparatus.

Abbreviations used in this paper: DAG, diacylglycerol; IQ, ilimaquinone; PKD, protein kinase D; VSV, vesicular stomatitis virus.


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