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一个新型的 AP-1 结合基序位于棕榈酰化的反式高尔基体网络/内体辅助蛋白 Gadkin/γ-BAR 内。

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

机构信息

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.

出版信息

J Biol Chem. 2010 Feb 5;285(6):4074-4086. doi: 10.1074/jbc.M109.049197. Epub 2009 Dec 3.

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.

摘要

网格蛋白-衔接蛋白 1(AP-1)衔接复合物包被小泡的组装部分介导了高尔基体反面管网(TGN)和内体之间的膜运输。这个过程涉及多个辅助蛋白,它们通过与 AP-1γ的耳域结合的退化肽基序直接结合到 AP-1γ上,这些基序符合共有序列 diameterG(P/D/E)(diameter/L/M)(其中 diameter 是一个大的疏水性氨基酸)。最近,γ-BAR(以下简称 Gadkin,原因将在下面解释)已被确定为一种新的 AP-1 募集因子,参与了溶酶体酶依赖于 AP-1 的内体运输。Gadkin 如何与膜和 AP-1γ精确相互作用仍然不清楚。在这里,我们表明 Gadkin 是一种 S-棕榈酰化的外周膜蛋白,缺乏稳定的三级结构。S-棕榈酰化是 Gadkin 募集到 TGN/内体膜所必需的,但不是与 AP-1 结合所必需的。此外,我们在内源性 Gadkin 中鉴定出一种新型的 AP-1 结合基序,它与 γ1-衔接蛋白的耳域特异性结合。该新型基序的突变失活,无论是单独失活还是与另外三个更传统的 AP-1γ结合肽一起失活,都会导致 Gadkin 错误定位到质膜,并干扰其使 AP-1 对布雷非德菌素 A 产生抗性的能力,表明其具有生理重要性。因此,我们的研究揭示了 Gadkin 介导的 AP-1 募集到 TGN/内体膜的分子基础,并确定了 AP-1 结合基序的一种新型亚型。

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