Leptosphaeria maculans Effector Protein AvrLm1 Modulates Plant Immunity by Enhancing MAP Kinase 9 Phosphorylation

First author: Lisong Ma; Affiliations: Saskatoon Research and Development Centre (加拿大农业部萨斯卡通研发中心): Saskatoon, Canada

Corresponding author: M. Hossein Borhan

Leptosphaeria maculans, the causal agent of blackleg disease (黑胫病) in canola (Brassica napus), secretes an array of effectors into the host to overcome host defense. Here we present evidence that the L. maculans effector protein AvrLm1 functions as a virulence factor by interacting with the B. napus mitogen-activated protein (MAP; 丝裂原活化蛋白) kinase 9 (BnMPK9), resulting in increased accumulation and enhanced phosphorylation of the host protein. Transient expression of BnMPK9 in Nicotiana benthamiana (烟草) induces cell death, and this phenotype is enhanced in the presence of AvrLm1, suggesting that induction of cell death due to enhanced accumulation and phosphorylation of BnMPK9 by AvrLm1 supports the initiation of necrotrophic phase (坏死营养阶段) of L. maculans infection. Stable expression of BnMPK9 in B. napus perturbs hormone signaling, notably salicylic acid response genes, to facilitate L. maculans infection. Our findings provide evidence that a MAP kinase is directly targeted by a fungal effector to modulate plant immunity.

Leptosphaeria maculans是导致油菜黑胫病的罪魁祸首，其能释放一批效应物到寄主中来克服寄主的抗性。本文的研究显示L. maculans的效应物AvrLm1作为毒力因子与油菜的丝裂原活化蛋白激酶BnMPK9互作，导致寄主蛋白的积累增加及磷酸化增强。对烟草进行BnMPK9遗传转化试验诱导了细胞死亡，并且这种表型会在存在AvrLm1的情况下得到增强，说明AvrLm1促进的BnMPK9蛋白积累增加和磷酸化增强会诱导细胞死亡，最终导致L. maculans侵染进入坏死营养阶段。油菜中BnMPK9基因的稳定表达会干扰激素的信号转导，尤其是水杨酸响应基因，从而促进L. maculans的侵染。本文的发现证明了一个真菌效应物会直接靶向MAP激酶从而调节植物的免疫。

通讯：M. Hossein Borhan（http://www.agr.gc.ca/eng/science-and-innovation/research-centres-and-collections/saskatchewan/saskatoon-research-and-development-centre/scientific-staff-and-expertise/borhan-hossein-phd/?id=1322853119549）

研究方向：植物响应病原菌的功能基因组学；植物病原菌基因组学。

doi: https://doi.org/10.1016/j.isci.2018.04.015

Journal: iScience

Published date: 21 April, 2018

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