Programmed cell death (PCD) pathways are found in many phyla, ranging from developmentally programmed apoptosis in animals to cell-autonomous programmed necrosis pathways that limit the spread of biotrophic pathogens in multicellular assemblies. Prominent examples for the latter include animal necroptosis and pyroptosis, plant hypersensitive response (HR), and fungal heterokaryon incompatibility (HI) pathways. PCD pathways in the different kingdoms show fundamental differences in execution mechanism, morphology of the dying cells, and in the biological sequelae. Nevertheless, recent studies have revealed remarkable evolutionary parallels, including a striking sequence relationship between the “HeLo” domains found in the pore-forming components of necroptosis and some types of plant HR and fungal HI pathways. Other PCD execution components show cross-kingdom conservation as well, or are derived from prokaryotic ancestors. The currently available data suggest a model, wherein the primordial eukaryotic PCD pathway used proteins similar to present-day plant R-proteins and caused necrotic cell death by direct action of Toll and IL-1 receptor (TIR) and HeLo-like domains.

中文翻译：

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程序性细胞死亡信号的进化起源。

程序性细胞死亡 (PCD) 途径存在于许多门中，从动物的发育程序性细胞凋亡到限制生物营养性病原体在多细胞组装中传播的细胞自主程序性坏死途径。后者的突出例子包括动物坏死性凋亡和细胞焦亡、植物过敏反应 (HR) 和真菌异核体不相容 (HI) 途径。不同领域的 PCD 通路在执行机制、垂死细胞的形态和生物学后遗症方面表现出根本差异。然而，最近的研究揭示了显着的进化相似性，包括在坏死性凋亡的成孔成分中发现的“HeLo”结构域与某些类型的植物 HR 和真菌 HI 途径之间存在惊人的序列关系。其他 PCD 执行组件也显示出跨界保护，或者源自原核祖先。目前可用的数据提出了一个模型，其中原始真核 PCD 途径使用类似于当今植物 R 蛋白的蛋白质，并通过 Toll 和 IL-1 受体 (TIR) 和 HeLo 样结构域的直接作用导致坏死细胞死亡。