State Key Laboratory for Crop Stress Resistance and High-Efficiency Production, College of Plant Protection, Northwest A&F University, Yangling, 712100, Shaanxi, China.
Department of Plant Pathology, College of Plant Protection, China Agricultural University, 2 Yuanmingyuanxi Road, Beijing, 100193, China.
Nat Commun. 2024 Mar 4;15(1):1967. doi: 10.1038/s41467-024-46290-z.
Host-derived reactive oxygen species (ROS) are an important defense means to protect against pathogens. Although mitochondria are the main intracellular targets of ROS, how pathogens regulate mitochondrial physiology in response to oxidative stress remains elusive. Prohibitin 2 (PHB2) is an inner mitochondrial membrane (IMM) protein, recognized as a mitophagy receptor in animals and fungi. Here, we find that an ANK and FYVE domain-containing protein PsAF5, is an adapter of PsPHB2, interacting with PsATG8 under ROS stress. Unlike animal PHB2 that can recruit ATG8 directly to mitochondria, PsPHB2 in Phytophthora sojae cannot recruit PsATG8 to stressed mitochondria without PsAF5. PsAF5 deletion impairs mitophagy under ROS stress and increases the pathogen's sensitivity to HO, resulting in the attenuation of P. sojae virulence. This discovery of a PsPHB2-PsATG8 adapter (PsAF5) in plant-pathogenic oomycetes reveals that mitophagy induction by IMM proteins is conserved in eukaryotes, but with differences in the details of ATG8 recruitment.
宿主来源的活性氧（ROS）是一种重要的防御手段，可用于抵御病原体。尽管线粒体是 ROS 的主要细胞内靶标，但病原体如何调节线粒体生理以应对氧化应激仍不清楚。PHB2 是一种线粒体内膜（IMM）蛋白，在动物和真菌中被认为是自噬受体。在这里，我们发现一种含有 ANK 和 FYVE 结构域的蛋白 PsAF5 是 PsPHB2 的衔接蛋白，在 ROS 应激下与 PsATG8 相互作用。与可以直接将 ATG8 募集到线粒体的动物 PHB2 不同，大豆疫霉菌中的 PsPHB2 在没有 PsAF5 的情况下无法将 PsATG8 募集到应激线粒体。PsAF5 缺失会损害 ROS 应激下的自噬作用，并增加病原体对 HO 的敏感性，从而降低大豆疫霉菌的毒力。在植物病原卵菌中发现的 PsPHB2-PsATG8 衔接蛋白（PsAF5）揭示了 IMM 蛋白诱导自噬在真核生物中是保守的，但在 ATG8 募集的细节上存在差异。
