A novel subtype of AP-1-binding motif within the palmitoylated trans-Golgi network/endosomal accessory protein Gadkin/gamma-BAR.

J Biol Chem

From the Institute of Chemistry and Biochemistry, Department of Membrane Biochemistry, Freie Universität and Charité-Universitätsmedizin Berlin, Takustrasse 6, 14195 Berlin, Germany; the Leibniz-Institut für Molekulare Pharmakologie, Robert-Rössle-Strasse 10, 13125 Berlin, Germany. Electronic address:

Published: February 2010

AI Article Synopsis

  • Membrane traffic between the trans-Golgi network and endosomes involves clathrin-AP-1 adaptor complex-coated vesicles, with Gadkin identified as a key recruitment factor for AP-1 in lysosomal enzyme trafficking.
  • Gadkin is characterized as an S-palmitoylated peripheral membrane protein that is essential for its localization to TGN/endosomal membranes but does not require S-palmitoylation for AP-1 binding.
  • A new subtype of the AP-1-binding motif within Gadkin has been discovered, with its alteration causing incorrect localization and impaired function in AP-1 recruitment, highlighting its physiological significance.

Article Abstract

Membrane traffic between the trans-Golgi network (TGN) and endosomes is mediated in part by the assembly of clathrin-AP-1 adaptor complex-coated vesicles. This process involves multiple accessory proteins that directly bind to the ear domain of AP-1gamma via degenerate peptide motifs that conform to the consensus sequence diameterG(P/D/E)(diameter/L/M) (with diameter being a large hydrophobic amino acid). Recently, gamma-BAR (hereafter referred to as Gadkin for reasons explained below) has been identified as a novel AP-1 recruitment factor involved in AP-1-dependent endosomal trafficking of lysosomal enzymes. How precisely Gadkin interacts with membranes and with AP-1gamma has remained unclear. Here we show that Gadkin is an S-palmitoylated peripheral membrane protein that lacks stable tertiary structure. S-Palmitoylation is required for the recruitment of Gadkin to TGN/endosomal membranes but not for binding to AP-1. Furthermore, we identify a novel subtype of AP-1-binding motif within Gadkin that specifically associates with the gamma1-adaptin ear domain. Mutational inactivation of this novel type of motif, either alone or in combination with three more conventional AP-1gamma binding peptides, causes Gadkin to mislocalize to the plasma membrane and interferes with its ability to render AP-1 brefeldin A-resistant, indicating its physiological importance. Our studies thus unravel the molecular basis for Gadkin-mediated AP-1 recruitment to TGN/endosomal membranes and identify a novel subtype of the AP-1-binding motif.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2823548PMC
http://dx.doi.org/10.1074/jbc.M109.049197DOI Listing

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