Selective autophagy underlies many of the important physiological roles that autophagy plays in multicellular organisms, but the mechanisms involved in cargo selection are poorly understood. Here we describe a molecular mechanism that can target conventional endosomes for autophagic degradation. We show that the human transmembrane protein TMEM59 contains a minimal 19-amino-acid peptide in its intracellular domain that promotes LC3 labelling and lysosomal targeting of its own endosomal compartment. Interestingly, this peptide defines a novel protein motif that mediates interaction with the WD-repeat domain of ATG16L1, thus providing a mechanistic basis for the activity. The motif is represented with the same ATG16L1-binding ability in other molecules, suggesting a more general relevance. We propose that this motif may play an important role in targeting specific membranous compartments for autophagic degradation, and therefore it may facilitate the search for adaptor proteins that promote selective autophagy by engaging ATG16L1. Endogenous TMEM59 interacts with ATG16L1 and mediates autophagy in response to Staphylococcus aureus infection.

译文

选择性自噬是自噬在多细胞生物中发挥的许多重要生理作用的基础,但是对货物选择所涉及的机制知之甚少。在这里,我们描述了一种分子机制,该机制可以靶向常规内体进行自噬降解。我们显示,人跨膜蛋白TMEM59在其细胞内结构域中包含最小19个氨基酸的肽,可促进LC3标记和溶酶体靶向其自身的内体区室。有趣的是,该肽定义了一种新型的蛋白质基序,该基序介导与ATG16L1的WD重复结构域的相互作用,从而为该活性提供了机械基础。该基序在其他分子中以相同的ATG16L1-binding能力表示,表明更普遍的相关性。我们认为,该基序可能在靶向特定的膜区室进行自噬降解中起重要作用,因此,它可能有助于寻找通过参与ATG16L1促进选择性自噬的衔接子蛋白。内源性TMEM59与ATG16L1相互作用并介导自噬以响应金黄色葡萄球菌感染。

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