Kelps are key primary producers of cold and temperate marine coastal ecosystems and exhibit systemic defences against pathogens. Yet, the cellular mechanisms underpinning their immunity remain to be elucidated. We investigated the time course of infection of the kelp Macrocystis pyrifera by the oomycete Anisolpidium ectocarpii using TEM, in vivo autophagy markers and autophagy inhibitors. Over several infection cycles, A. ectocarpii undergoes sequential physiological shifts sensitive to autophagy inhibitors. Initially lipid-rich, pathogen thalli become increasingly lipid-depleted; they subsequently tend to become entirely abortive, irrespective of their lipid content. Moreover, infected algal cells mount local defences and can directly eliminate the pathogen by xenophagy. Finally, autophagy-dependent plastid recycling is induced in uninfected host cells. We demonstrate the existence of local, inducible autophagic processes both in the pathogen and infected host cells, which result in the restriction of pathogen propagation. We also show the existence of a systemic algal response mediated by autophagy. We propose a working model accounting for all our observations, whereby the outcome of the algal-pathogen interaction (i.e. completion or not of the pathogen life cycle) is dictated by the induction, and possibly the mutual hijacking, of the host and pathogen autophagy machineries.

中文翻译：

---

寄主和病原体自噬是巨海藻巨藻海藻对卵菌病原体Anisolpidium ectocarpii的可诱导局部防御和系统反应的关键。

海带是寒冷和温带海洋沿海生态系统的主要主要生产者，对病原体具有系统的防御能力。然而，支撑其免疫力的细胞机制仍有待阐明。我们使用透射电镜，体内自噬标记和自噬抑制剂研究了卵菌无皮茴香（Anisolpidium ectocarpii）感染紫菜海带Macrocystis pyrifera的时间过程。在几个感染周期中，果皮农杆菌经历了对自噬抑制剂敏感的连续生理转变。最初富含脂质的病原体thalli变得越来越缺乏脂质。他们随后倾向于完全流产，而不论其脂质含量如何。此外，被感染的藻类细胞具有局部防御能力，可以通过异种吞噬直接消除病原体。最后，在未感染的宿主细胞中诱导自噬依赖性质体循环。我们证明了在病原体和被感染的宿主细胞中都存在局部可诱导的自噬过程，这导致了病原体繁殖的限制。我们还显示了由自噬介导的系统性藻类反应的存在。我们提出了一个工作模型，说明了我们的所有观察结果，藻类-病原体相互作用的结果（即病原体生命周期的完成与否）由宿主和病原体自噬机器的诱导以及可能的相互劫持决定。 。我们还显示了由自噬介导的系统性藻类反应的存在。我们提出了一个工作模型，说明了我们的所有观察结果，藻类-病原体相互作用的结果（即病原体生命周期的完成与否）由宿主和病原体自噬机器的诱导以及可能的相互劫持决定。 。我们还显示了由自噬介导的系统性藻类反应的存在。我们提出了一个工作模型，说明了我们的所有观察结果，藻类-病原体相互作用的结果（即病原体生命周期的完成与否）由宿主和病原体自噬机器的诱导以及可能的相互劫持决定。 。