今天,介紹本周發表在plos pathegons上,德國哥廷根哥廷根大學發表的研究論文《Signal peptide peptidase activity connects the unfolded protein response to plant defense suppression by Ustilago maydis》。
玉米黑穗病真菌Ustilago maydis需要未摺疊蛋白反應(UPR)以在與玉米的活體營養型相互作用期間維持內質網(ER)的穩態。UPR和控制致病性發展的途徑之間的相互作用由UPR調節子Cib1和發育調節因子Clp1之間的相互作用介導。Cib1 / Clp1複合物形成導致調控網絡的修飾,從而使植物中的真菌增殖,效應子分泌與ER脅迫耐受性的增強和植物中的長期UPR激活相一致。
在本文中,作者使用RNAseq / ChIPseq聯合分析解決UPR依賴性基因表達及其通過Clp1的調節。ER應激抗性的增強與Cp1磷酸化,蛋白質穩定性和UPR基因表達的Clp1依賴性改變有關。重要的是,通過刪除UPR核心基因,篩選到信號肽肽酶Spp1是玉米黑穗菌與其宿主玉米之間建立相容的活體營養相互作用所需的新關鍵因子。Spp1對於ER脅迫抗性和營養生長是不必要的,但是需要催化活性來幹擾植物防禦,揭示了活體營養真菌/植物相互作用中信號肽肽酶的新的毒力特異性功能。
The corn smut fungus Ustilago maydis requires the unfolded protein response (UPR) to maintain homeostasis of the endoplasmic reticulum (ER) during the biotrophic interaction with its host plant Zea mays (maize). Crosstalk between the UPR and pathways controlling pathogenic development is mediated by protein-protein interactions between the UPR regulator Cib1 and the developmental regulator Clp1. Cib1/Clp1 complex formation results in mutual modification of the connected regulatory networks thereby aligning fungal proliferation in planta, efficient effector secretion with increased ER stress tolerance and long-term UPR activation in planta. Here we address UPR-dependent gene expression and its modulation by Clp1 using combinatorial RNAseq/ChIPseq analyses. We show that increased ER stress resistance is connected to Clp1-dependent alterations of Cib1 phosphorylation, protein stability and UPR gene expression. Importantly, we identify by deletion screening of UPR core genes the signal peptide peptidase Spp1 as a novel key factor that is required for establishing a compatible biotrophic interaction between U. maydis and its host plant maize. Spp1 is dispensable for ER stress resistance and vegetative growth but requires catalytic activity to interfere with the plant defense, revealing a novel virulence specific function for signal peptide peptidases in a biotrophic fungal/plant interaction.
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"植物病毒與抗逆研究"由浙江大學植物病理學博士研究生黑暗大邪神管理與運營。
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