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WKS1/Yr36 通过磷酸化 KAT-2B 将脂质通量重新导向茉莉酸以增强对小麦条锈病的抗性。

Phosphorylation of KAT-2B by WKS1/Yr36 redirects the lipid flux to jasmonates to enhance resistance against wheat stripe rust.

机构信息

Frontiers Science Center for Molecular Design Breeding (MOE), China Agricultural University, Beijing 100193, China; Xianghu Laboratory, Hangzhou, Zhejiang 311231, China; School of Life Sciences, Fudan University, Shanghai 200438, China.

School of Life Sciences, Fudan University, Shanghai 200438, China.

出版信息

J Genet Genomics. 2023 Nov;50(11):872-882. doi: 10.1016/j.jgg.2023.08.009. Epub 2023 Sep 2.

DOI:10.1016/j.jgg.2023.08.009
PMID:37666356
Abstract

Wheat (Triticum aestivum) is one of the most essential human energy and protein sources. However, wheat production is threatened by devastating fungal diseases such as stripe rust, caused by Puccinia striiformis Westend. f. sp. tritici (Pst). Here, we reveal that the alternations in chloroplast lipid profiles and the accumulation of jasmonate (JA) in the necrosis region activate JA signaling and trigger the host defense. The collapse of chloroplasts in the necrosis region results in accumulations of polyunsaturated membrane lipids and the lipid-derived phytohormone JA in transgenic lines of Yr36 that encodes Wheat Kinase START 1 (WKS1), a high-temperature-dependent adult plant resistance protein. WKS1.1, a protein encoded by a full-length splicing variant of WKS1, phosphorylates and enhances the activity of keto-acyl thiolase (KAT-2B), a critical enzyme catalyzing the β-oxidation reaction in JA biosynthesis. The premature stop mutant, kat-2b, accumulates less JA and shows defects in the host defense against Pst. Conversely, overexpression of KAT-2B results in a higher level of JA and limits the growth of Pst. Moreover, JA inhibits the growth and reduces pustule densities of Pst. This study illustrates the WKS1.1‒KAT-2B‒JA pathway for enhancing wheat defense against fungal pathogens to attenuate yield loss.

摘要

小麦(Triticum aestivum)是人类最重要的能量和蛋白质来源之一。然而,小麦生产受到毁灭性真菌病害的威胁,例如条锈病,由条形柄锈菌(Puccinia striiformis Westend. f. sp. tritici)引起。在这里,我们揭示了叶绿体脂质谱的变化和坏死区域茉莉酸(JA)的积累激活了 JA 信号通路并引发了宿主防御。坏死区域的叶绿体崩溃导致多不饱和膜脂质和脂质衍生的植物激素 JA 在编码小麦激酶起始 1(WKS1)的 Yr36 转基因系中的积累,WKS1 是一种高温依赖的成株期抗性蛋白。WKS1.1 是 WKS1 的全长剪接变体编码的一种蛋白质,可磷酸化并增强酮酰硫解酶(KAT-2B)的活性,KAT-2B 是 JA 生物合成中β-氧化反应的关键酶。过早停止突变体 kat-2b 积累的 JA 较少,并且在对 Pst 的宿主防御中存在缺陷。相反,KAT-2B 的过表达会导致 JA 水平升高,并限制 Pst 的生长。此外,JA 抑制 Pst 的生长并降低其疱斑密度。本研究说明了 WKS1.1-KAT-2B-JA 途径可增强小麦对真菌病原体的防御能力,从而减轻产量损失。

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