廣譜抗性調控是植物生物學研究的一個活躍領域。抗白粉病8.1(RPW8.1)是引發過敏反應(HR)以限制多重致病性感染的少數廣譜抗病基因之一。為了解決 RPW8.1信號是如何調控的問題,我們進行了一個基因篩選,並試圖確定突變增強 RPW8.1介導的 HR。在這裡,我們提供了證據連接膜聯蛋白與 RPW8.1介導的抗白粉病的擬南芥。我們分離並鑑定了擬南芥 b7-6突變體。At5g12380位點的 b7-6突變導致 ANNEXIN 8(AtANN8)發生胺基酸替換。AtANN8基因功能缺失或 RNA 沉默導致 RPW8.1、 RPW8.1依賴性壞死灶在葉片中的表達增強,並對白粉病進行防禦。相反,過度表達 AtANN8會損害 RPW8.1介導的抗病性和細胞死亡。有趣的是,AtANN8的突變增強了 RPW8.1觸發 H2O2。此外,AtANN8基因的突變導致了過敏的鹽脅迫。總之,我們的數據表明,AtANN8參與多種逆境信號通路,負調節 RPW8.1介導的抗白粉病和細胞死亡,從而將 ANNEXIN 的功能與植物免疫聯繫起來。
Study on the regulation of broad‐spectrum resistance is an active area in plant biology. RESISTANCE TO POWDERY MILDEW 8.1 (RPW8.1) is one of a few broad‐spectrum resistance genes triggering the hypersensitive response (HR) to restrict multiple pathogenic infections. To address the question how RPW8.1 signaling is regulated, we performed a genetic screen and tried to identify mutations enhancing RPW8.1‐mediated HR. Here, we provided evidence to connect an annexin protein with RPW8.1‐mediated resistance in Arabidopsis against powdery mildew. We isolated and characterized Arabidopsis b7‐6 mutant. A point mutation in b7‐6 at the At5g12380 locus resulted in an amino acid substitution in ANNEXIN 8 (AtANN8). Loss‐of‐function or RNA‐silencing of AtANN8 led to enhanced expression of RPW8.1, RPW8.1‐dependent necrotic lesions in leaves, and defense against powdery mildew. Conversely, over‐expression of AtANN8 compromised RPW8.1‐mediated disease resistance and cell death. Interestingly, the mutation in AtANN8 enhanced RPW8.1‐triggered H2O2. In addition, mutation in AtANN8 led to hypersensitivity to salt stress. Together, our data indicate that AtANN8 is involved in multiple stress signaling pathways and negatively regulates RPW8.1‐mediated resistance against powdery mildew and cell death, thus linking ANNEXIN's function with plant immunity.
Zhao, Z.‐X., Xu, Y.‐J., Lei, Y., Li, Q., Zhao, J.‐Q., Li, Y., Fan, J., Xiao, S. and Wang, W.‐M. (2020), ANNEXIN 8 negatively regulates RPW8.1‐mediated cell death and disease resistance in Arabidopsis. J. Integr. Plant Biol. Accepted Author Manuscript. doi:10.1111/jipb.13025
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