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GABARAP与ATG3背面相互作用及无配体ATG3构象的结构见解

Structural Insights into the GABARAP-ATG3 Backside Interaction and Apo ATG3 Conformation.

作者信息

Ohashi Kazuto, Kroon Gerard J, Otomo Takanori

机构信息

Department of Integrative Structural and Computational Biology, The Scripps Research Institute, 10550 North Torrey Pines Rd, La Jolla, California 92037, United States.

Institute for Molecular and Cellular Regulation, Gunma University, 371-8512 Gunma, Japan.

出版信息

Biochemistry. 2025 Aug 5;64(15):3178-3189. doi: 10.1021/acs.biochem.4c00485. Epub 2025 Jul 8.

Abstract

Members of the ATG8 family of ubiquitin-like proteins (Ubls) are covalently attached to phosphatidylethanolamine (PE) on nascent autophagosomal membranes, where they recruit cargo receptors and promote membrane expansion. Although the overall lipidation pathway is well established, the molecular details-particularly those involving the E2 enzyme ATG3-remain incompletely defined. Here, we uncover a previously unrecognized, noncovalent binding mode between the mammalian ATG8 protein GABARAP and the backside of ATG3's catalytic E2 domain. In crystals, an isopeptide-linked GABARAP∼ATG3 conjugate self-assembles into a helical filament via this backside interface, mirroring architectures observed for canonical Ub/Ubl∼E2 conjugates. The E2 backside-binding surface on GABARAP is topologically distinct from those of other Ub/Ubl proteins and overlaps the LC3-interacting region (LIR) motif-binding site. Solution NMR confirms this interaction, and targeted mutagenesis shows that disrupting the interface impairs PE conjugation. Complementary NMR and AlphaFold modeling of apo ATG3 reveal an intramolecular contact between a segment of its flexible region (FR) and the catalytic core that suppresses conjugation. Together, these findings establish backside engagement as a critical feature of ATG8 lipidation and illuminate the dynamic architecture and regulation of ATG3.

摘要

泛素样蛋白(Ubls)的自噬相关基因8(ATG8)家族成员共价连接到新生自噬体膜上的磷脂酰乙醇胺(PE)上,在那里它们招募货物受体并促进膜扩张。尽管整体脂化途径已得到充分确立,但分子细节,特别是那些涉及E2酶ATG3的细节,仍未完全明确。在这里,我们发现了哺乳动物ATG8蛋白γ-氨基丁酸A型受体相关蛋白(GABARAP)与ATG3催化E2结构域背面之间一种以前未被认识的非共价结合模式。在晶体中,一种异肽连接的GABARAP∼ATG3共轭物通过这个背面界面自组装成螺旋丝,这与经典泛素/泛素样蛋白∼E2共轭物所观察到的结构相似。GABARAP上的E2背面结合表面在拓扑结构上与其他泛素/泛素样蛋白不同,并且与LC3相互作用区域(LIR)基序结合位点重叠。溶液核磁共振(NMR)证实了这种相互作用,靶向诱变表明破坏该界面会损害PE共轭。对无apo ATG3的互补NMR和AlphaFold建模揭示了其柔性区域(FR)的一个片段与催化核心之间的分子内接触,该接触抑制共轭。总之,这些发现确立了背面结合是ATG8脂化的一个关键特征,并阐明了ATG3的动态结构和调控。

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