Indole-3-acetaldehyde dehydrogenase-dependent auxin synthesis contributes to virulence of Pseudomonas syringae strain DC3000.

Indole-3-acetaldehyde dehydrogenase-dependent auxin synthesis contributes to virulence of Pseudomonas syringae strain DC3000.
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DOI:
10.1371/journal.ppat.1006811
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发表时间:
2018-01
期刊:
影响因子:
6.7
通讯作者:
Kunkel BN
Kunkel BN
中科院分区:
医学1区
文献类型:
--
作者:
McClerklin SA;Lee SG;Harper CP;Nwumeh R;Jez JM;Kunkel BN

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细菌病原体假单胞菌调节植物激素信号以促进感染和疾病发展。P. arabidingae使用几种策略来操纵拟南芥中的生长素生理学以促进致病性,包括其合成吲哚-3-乙酸(IAA)(植物中生长素的主要形式)和产生改变宿主中生长素反应的毒力因子;然而,病原体来源的生长素在P. arabidingae致病性中的作用尚不清楚。在这里,我们证明了P. dichingae菌株DC 3000通过以前未表征的途径产生IAA,并确定了一种新的吲哚-3-乙醛脱氢酶,AldA,其在IAA生物合成中的功能是通过催化NAD依赖性的吲哚-3-乙醛(IAAld)形成IAA。生化分析和解决1.9毫米分辨率的X射线晶体结构揭示了关键特征的AldA的IAA合成,包括底物特异性的分子基础。破坏aldA和一个相近的同源物aldB,导致培养物中IAA产量减少,对A. thaliana.我们使用这些突变体来探索病原体来源的生长素有助于毒力的机制,并表明DC 3000产生的IAA抑制水杨酸介导的防御。thaliana.因此,生长素是DC 3000毒力因子,其通过抑制宿主防御来促进致病性。病原体已经进化出多种策略来抑制宿主防御和调节宿主生理以促进定殖和疾病发展。例如,植物病原体假单胞菌使用几种策略来操纵其宿主的激素信号传导,包括产生改变植物激素或激素模拟物的激素反应和合成的毒力因子。吲哚-3-乙酸(IAA)是植物激素生长素的一种常见形式,许多植物病原体的合成与毒力有关。然而,病原体衍生的IAA在叶斑病病原体如P. lingae菌株DC 3000的致病过程中的作用还没有很好地理解。在这里,我们证明,P. dichingae菌株DC 3000使用以前未表征的生化途径来合成IAA,催化的一种新的醛脱氢酶,AldA,并进行生化和结构研究的AldA蛋白质调查AldA活性和底物特异性。我们还产生了一个破坏IAA合成的aldA突变体,以表明IAA是一种DC 3000毒力因子,通过抑制宿主防御反应来促进发病。
The bacterial pathogen Pseudomonas syringae modulates plant hormone signaling to promote infection and disease development. P. syringae uses several strategies to manipulate auxin physiology in Arabidopsis thaliana to promote pathogenesis, including its synthesis of indole-3-acetic acid (IAA), the predominant form of auxin in plants, and production of virulence factors that alter auxin responses in the host; however, the role of pathogen-derived auxin in P. syringae pathogenesis is not well understood. Here we demonstrate that P. syringae strain DC3000 produces IAA via a previously uncharacterized pathway and identify a novel indole-3-acetaldehyde dehydrogenase, AldA, that functions in IAA biosynthesis by catalyzing the NAD-dependent formation of IAA from indole-3-acetaldehyde (IAAld). Biochemical analysis and solving of the 1.9 Å resolution x-ray crystal structure reveal key features of AldA for IAA synthesis, including the molecular basis of substrate specificity. Disruption of aldA and a close homolog, aldB, lead to reduced IAA production in culture and reduced virulence on A. thaliana. We use these mutants to explore the mechanism by which pathogen-derived auxin contributes to virulence and show that IAA produced by DC3000 suppresses salicylic acid-mediated defenses in A. thaliana. Thus, auxin is a DC3000 virulence factor that promotes pathogenicity by suppressing host defenses. Pathogens have evolved multiple strategies for suppressing host defenses and modulating host physiology to promote colonization and disease development. For example, the plant pathogen Pseudomonas syringae uses several strategies to the manipulate hormone signaling of its hosts, including production of virulence factors that alter hormone responses in and synthesis of plant hormones or hormone mimics. Synthesis of indole-3-acetic acid (IAA), a common form of the plant hormone auxin, by many plant pathogens has been implicated in virulence. However, the role of pathogen-derived IAA during pathogenesis by leaf spotting pathogens such as P. syringae strain DC3000 is not well understood. Here, we demonstrate that P. syringae strain DC3000 uses a previously uncharacterized biochemical pathway to synthesize IAA, catalyzed by a novel aldehyde dehydrogenase, AldA, and carry out biochemical and structural studies of the AldA protein to investigate AldA activity and substrate specificity. We also generate an aldA mutant disrupted in IAA synthesis to show that IAA is a DC3000 virulence factor that promotes pathogenesis by suppressing host defense responses.
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