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奇异果细菌定植者之间不同的效应子谱揭示了在抑制PTI和RIN4方面趋同的冗余作用。

Contrasting effector profiles between bacterial colonisers of kiwifruit reveal redundant roles converging on PTI-suppression and RIN4.

作者信息

Jayaraman Jay, Yoon Minsoo, Hemara Lauren M, Bohne Deborah, Tahir Jibran, Chen Ronan K Y, Brendolise Cyril, Rikkerink Erik H A, Templeton Matthew D

机构信息

The New Zealand Institute for Plant and Food Research Ltd, Mt. Albert Research Centre, Auckland, 1025, New Zealand.

School of Biological Sciences, University of Auckland, Auckland, 1010, New Zealand.

出版信息

New Phytol. 2023 May;238(4):1605-1619. doi: 10.1111/nph.18848. Epub 2023 Mar 20.

DOI:10.1111/nph.18848
PMID:36856342
Abstract

Testing effector knockout strains of the Pseudomonas syringae pv. actinidiae biovar 3 (Psa3) for reduced in planta growth in their native kiwifruit host revealed a number of nonredundant effectors that contribute to Psa3 virulence. Conversely, complementation in the weak kiwifruit pathogen P. syringae pv. actinidifoliorum (Pfm) for increased growth identified redundant Psa3 effectors. Psa3 effectors hopAZ1a and HopS2b and the entire exchangeable effector locus (ΔEEL; 10 effectors) were significant contributors to bacterial colonisation of the host and were additive in their effects on virulence. Four of the EEL effectors (HopD1a, AvrB2b, HopAW1a and HopD2a) redundantly contribute to virulence through suppression of pattern-triggered immunity (PTI). Important Psa3 effectors include several redundantly required effectors early in the infection process (HopZ5a, HopH1a, AvrPto1b, AvrRpm1a and HopF1e). These largely target the plant immunity hub, RIN4. This comprehensive effector profiling revealed that Psa3 carries robust effector redundancy for a large portion of its effectors, covering a few functions critical to disease.

摘要

对猕猴桃溃疡病菌丁香假单胞菌猕猴桃致病变种3(Psa3)的效应子敲除菌株在其天然猕猴桃宿主中进行体内生长能力降低的测试,发现了许多对Psa3毒力有贡献的非冗余效应子。相反,在弱致病的猕猴桃病原菌丁香假单胞菌猕猴桃叶致病变种(Pfm)中进行互补以促进其生长,鉴定出了冗余的Psa3效应子。Psa3效应子hopAZ1a和HopS2b以及整个可交换效应子位点(ΔEEL;10个效应子)对宿主细菌定殖有显著贡献,并且它们对毒力的影响具有累加性。EEL效应子中的四个(HopD1a、AvrB2b、HopAW1a和HopD2a)通过抑制模式触发免疫(PTI)对毒力有冗余贡献。重要的Psa3效应子包括感染过程早期几个冗余所需的效应子(HopZ5a、HopH1a、AvrPto1b、AvrRpm1a和HopF1e)。这些效应子主要靶向植物免疫枢纽RIN4。这种全面的效应子分析表明,Psa3的大部分效应子具有强大的效应子冗余性,涵盖了对病害至关重要的一些功能。

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