关键词: Autophagy Biotrophy Effector Oomycete Vacuoles

Mesh : Phytophthora / physiology Autophagy Plant Diseases / microbiology parasitology Nicotiana / microbiology Autophagy-Related Protein 8 Family / metabolism genetics Host-Pathogen Interactions

来  源:   DOI:10.1186/s12915-024-01899-w   PDF(Pubmed)

Abstract:
BACKGROUND: Plant pathogens secrete effector proteins into host cells to suppress immune responses and manipulate fundamental cellular processes. One of these processes is autophagy, an essential recycling mechanism in eukaryotic cells that coordinates the turnover of cellular components and contributes to the decision on cell death or survival.
RESULTS: We report the characterization of AVH195, an effector from the broad-spectrum oomycete plant pathogen, Phytophthora parasitica. We show that P. parasitica expresses AVH195 during the biotrophic phase of plant infection, i.e., the initial phase in which host cells are maintained alive. In tobacco, the effector prevents the initiation of cell death, which is caused by two pathogen-derived effectors and the proapoptotic BAX protein. AVH195 associates with the plant vacuolar membrane system and interacts with Autophagy-related protein 8 (ATG8) isoforms/paralogs. When expressed in cells from the green alga, Chlamydomonas reinhardtii, the effector delays vacuolar fusion and cargo turnover upon stimulation of autophagy, but does not affect algal viability. In Arabidopsis thaliana, AVH195 delays the turnover of ATG8 from endomembranes and promotes plant susceptibility to P. parasitica and the obligate biotrophic oomycete pathogen Hyaloperonospora arabidopsidis.
CONCLUSIONS: Taken together, our observations suggest that AVH195 targets ATG8 to attenuate autophagy and prevent associated host cell death, thereby favoring biotrophy during the early stages of the infection process.
摘要:
背景:植物病原体将效应蛋白分泌到宿主细胞中以抑制免疫应答并操纵基本细胞过程。这些过程之一是自噬,真核细胞中一种重要的回收机制,它协调细胞成分的周转,并有助于决定细胞死亡或存活。
结果:我们报告了AVH195的特征,AVH195是广谱卵菌植物病原体的一种效应物,寄生疫霉。我们表明,寄生假单胞菌在植物感染的生物营养阶段表达AVH195,即,宿主细胞存活的初始阶段。在烟草中,效应子阻止细胞死亡的开始,这是由两种病原体来源的效应子和促凋亡的BAX蛋白引起的。AVH195与植物液泡膜系统相关,并与自噬相关蛋白8(ATG8)同工型/旁系同源物相互作用。当在来自绿藻的细胞中表达时,莱茵衣藻,效应子在刺激自噬时延迟液泡融合和货物周转,但不影响藻类的生存能力。在拟南芥中,AVH195延迟了ATG8从内膜的周转,并促进了植物对寄生假单胞菌和专性生物营养卵菌病原体的敏感性。
结论:综合来看,我们的观察表明,AVH195靶向ATG8以减弱自噬并防止相关的宿主细胞死亡,从而在感染过程的早期阶段有利于生物萎缩。
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