Pathogenic fungi neutralize plant-derived ROS via Srpk1 deacetylation.
Pathogenic fungi neutralize plant-derived ROS via Srpk1 deacetylation.
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DOI：
10.15252/embj.2022112634
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发表时间：
2023-05-02
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植物对病原菌的入侵反应是诱导活性氧的产生，从而抑制病原菌的入侵。反过来，适应的病原体已经进化出一种酶促ROS解毒的抵消机制，但它如何被激活仍然难以捉摸。在这里，我们表明，在番茄维管枯萎病病原体尖孢镰刀菌f。在番茄属（Fol）中，该过程由Folk1激酶的脱乙酰化引发。在ROS暴露后，Fol通过改变乙酰化控制酶的表达来降低K304残基上的Folk1乙酰化。脱乙酰Folk1从细胞质FolAha1蛋白中解离，从而使其能够核转位。Folk1在细胞核中的积累增加使得其磷酸化靶FolSr1过度磷酸化，随后增强不同类型的抗氧化酶的转录。这些酶的分泌去除植物产生的H2O2，并使成功的Fol入侵。Folk1同源物的脱乙酰化在灰葡萄孢和可能的其他真菌病原体中具有类似的功能。这些发现揭示了植物真菌感染后启动ROS解毒的保守机制。番茄枯萎病菌侵染后活性氧的产生。番茄激活了一个真菌的R0S1依赖的ROS解毒程序。
In response to infection, plants can induce the production of reactive oxygen species (ROS) to restrict pathogen invasion. In turn, adapted pathogens have evolved a counteracting mechanism of enzymatic ROS detoxification, but how it is activated remains elusive. Here, we show that in the tomato vascular wilt pathogen Fusarium oxysporum f. sp. lycopersici (Fol) this process is initiated by deacetylation of the FolSrpk1 kinase. Upon ROS exposure, Fol decreases FolSrpk1 acetylation on the K304 residue by altering the expression of the acetylation‐controlling enzymes. Deacetylated FolSrpk1 disassociates from the cytoplasmic FolAha1 protein, thus enabling its nuclear translocation. Increased accumulation of FolSrpk1 in the nucleus allows for hyperphosphorylation of its phosphorylation target FolSr1 that subsequently enhances transcription of different types of antioxidant enzymes. Secretion of these enzymes removes plant‐produced H2O2, and enables successful Fol invasion. Deacetylation of FolSrpk1 homologs has a similar function in Botrytis cinerea and likely other fungal pathogens. These findings reveal a conserved mechanism for initiation of ROS detoxification upon plant fungal infection. ROS production in tomato plants infected by the pathogen Fusarium oxysporum f. sp. Lycopersici activates a fungal Srpk1‐dependent ROS detoxification program.