The apple FERONIA receptor-like kinase MdMRLK2 negatively regulates Valsa canker resistance by suppressing defence responses and hypersensitive reaction.
The apple FERONIA receptor-like kinase MdMRLK2 negatively regulates Valsa canker resistance by suppressing defence responses and hypersensitive reaction.
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DOI：
10.1111/mpp.13218
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发表时间：
2022-08
影响因子：
4.9
通讯作者：
Liu, Changhai
中科院分区：
文献类型：
--
作者：
Jing, Yuanyuan;Zhan, Minghui;Li, Chunrong;Pei, Tingting;Wang, Qi;Li, Pengmin;Ma, Fengwang;Liu, Changhai
苹果腐烂病是由苹果腐烂病（Valsa mali）引起的一种重要病害，在我国和东亚地区危害严重。植物受体样激酶FERONIA参与植物细胞的生长、发育和免疫。然而，关于FERONIA在苹果抗V. mali防御中的功能知之甚少。在这项研究中，我们发现MdMRLK 2在感病苹果的枝条中被苹果枯萎病高度诱导，而在抗病品种云南海棠的枝条中则没有。35 S：MdMRLK 2苹果植物相对于野生型（WT）植物显示出受损的抗性。进一步的分析表明，35 S：MdMRLK 2苹果植物相对于WT在苹果疫霉菌感染时具有增强的脱落酸（阿坝）水平和降低的水杨酸（SA）水平。MdMRLK 2过表达还抑制多酚积累，并抑制苯丙氨酸解氨酶（PAL）、β-1，3-葡聚糖酶（GLU）和几丁质酶（CHT）的活性。此外，MdMRLK 2与MdHIR 1（一种过敏诱导反应蛋白）相互作用，并抑制MdHIR 1介导的过敏反应（HR），可能是通过削弱MdHIR 1自身相互作用。总的来说，这些研究结果表明，MdMRLK 2的过表达可能通过（a）改变阿坝和SA水平，（B）抑制多酚积累，（c）抑制PAL，GLU和CHT活性，以及（d）通过破坏MdHIR 1自身相互作用来阻断MdHIR 1介导的HR来损害Valsa溃疡病抗性。苹果FERONIA受体样激酶MdMRLK 2通过改变脱落酸和水杨酸水平、抑制多酚积累、防御酶活性和过敏反应来负调节腐烂病溃疡病抗性。
Valsa canker, caused by the fungus Valsa mali, is one of the most destructive diseases of apple trees in China and other East Asian countries. The plant receptor‐like kinase FERONIA is involved in plant cell growth, development, and immunity. However, little is known about the function of FERONIA in apple defence against V. mali. In this study, we found that MdMRLK2 was highly induced by V. mali in twigs of V. mali‐susceptible Malus mellana but not in those of the resistant species Malus yunnaensis. 35S:MdMRLK2 apple plants showed compromised resistance relative to wild‐type (WT) plants. Further analyses indicated that 35S:MdMRLK2 apple plants had enhanced abscisic acid (ABA) levels and reduced salicylic acid (SA) levels relative to the WT on V. mali infection. MdMRLK2 overexpression also suppressed polyphenol accumulation and inhibited the activities of phenylalanine ammonia‐lyase (PAL), β‐1,3‐glucanase (GLU), and chitinase (CHT) during V. mali infection. Moreover, MdMRLK2 interacted with MdHIR1, a hypersensitive‐induced response protein, and suppressed the MdHIR1‐mediated hypersensitive reaction (HR), probably by impairing MdHIR1 self‐interaction. Collectively, these findings demonstrate that overexpression of MdMRLK2 compromises Valsa canker resistance, probably by (a) altering ABA and SA levels, (b) suppressing polyphenol accumulation, (c) inhibiting PAL, GLU, and CHT activities, and (d) blocking MdHIR1‐mediated HR by disrupting MdHIR1 self‐interaction. An apple FERONIA receptor‐like kinase, MdMRLK2, negatively regulates Valsa canker resistance by altering abscisic acid and salicylic acid levels, suppressing polyphenol accumulation, defence enzymes activities, and the hypersensitive reaction.
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