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External Lipid PI3P Mediates Entry of Eukaryotic Pathogen Effectors into Plant and Animal Host Cells

机译:外部脂质PI3P介导真核病原效应子进入植物和动物宿主细胞

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摘要

Pathogens of plants and animals produce effector proteins that are transferred into the cytoplasm of host cells to suppress host defenses. One type of plant pathogens, oomycetes, produces effector proteins with N-terminal RXLR and dEER motifs that enable entry into host cells. We show here that effectors of another pathogen type, fungi, contain functional variants of the RXLR motif, and that the oomycete and fungal RXLR motifs enable binding to the phospholipid, phosphatidylinositol-3-phosphate (PI3P). We find that PI3P is abundant on the outer surface of plant cell plasma membranes and, furthermore, on some animal cells. All effectors could also enter human cells, suggesting that PI3P-mediated effector entry may be very widespread in plant, animal and human pathogenesis. Entry into both plant and animal cells involves lipid raft-mediated endocytosis. Blocking PI3P binding inhibited effector entry, suggesting new therapeutic avenues.
机译:动植物的病原体产生效应蛋白,这些效应蛋白被转移到宿主细胞的细胞质中以抑制宿主防御。一种类型的植物病原体卵菌产生具有N末端RXLR和dEER基序的效应蛋白,使它们能够进入宿主细胞。我们在这里显示另一种病原体类型的效应物,真菌,包含RXLR主题的功能变体,卵菌和真菌RXLR主题能够与磷脂,磷脂酰肌醇-3-磷酸酯(PI3P)结合。我们发现PI3P在植物细胞质膜的外表面上丰富,而且在一些动物细胞上也丰富。所有效应子也可能进入人类细胞,这表明PI3P介导的效应子进入可能在植物,动物和人类发病机理中非常普遍。进入植物和动物细胞均涉及脂质筏介导的内吞作用。阻断PI3P结合抑制了效应子的进入,提示了新的治疗途径。

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