Dual Role of Auxin in Regulating Plant Defense and Bacterial Virulence Gene Expression During Pseudomonas syringae PtoDC3000 Pathogenesis.

Dual Role of Auxin in Regulating Plant Defense and Bacterial Virulence Gene Expression During Pseudomonas syringae PtoDC3000 Pathogenesis.
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DOI:
10.1094/mpmi-02-20-0047-r
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发表时间:
2020-08
期刊:
Molecular plant-microbe interactions : MPMI
影响因子:
--
通讯作者:
Kunkel BN
Kunkel BN
中科院分区:
其他
文献类型:
--
作者:
Djami-Tchatchou AT;Harrison GA;Harper CP;Wang R;Prigge MJ;Estelle M;Kunkel BN

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寄主激素生物学修饰是植物病原体促进病害的常见策略。例如,细菌病原体菌株假单胞菌DC 3000(PtoDC 3000)产生植物激素生长素(吲哚-3-乙酸[IAA])以促进PtoDC 3000在植物组织中的生长。以前的研究表明,生长素可能通过多种机制,包括抑制水杨酸(SA)介导的宿主防御和通过一个未知的机制,似乎是独立的SA促进PtoDC 3000的发病机制。为了测试宿主生长素信号传导在发病过程中是否重要,我们利用了生长素信号传导或感知受损的拟南芥品系。我们发现,在表达诱导型显性axr 2 -1突变的植物中,生长素信号传导的中断导致细菌生长减少,并且这种表型通过引入抑制SA合成的A12 -2突变而被抑制。因此,宿主生长素信号传导是PtoDC 3000正常易感性所必需的,并且参与抑制SA介导的防御。出乎意料的是,tir 1 afb 1 afb 4 afb 5四重突变体植物缺乏已知的六种生长素共受体中的四种,表现出生长素感知能力下降,支持细菌生长水平的增加。这种突变体表现出较高的IAA水平和降低SA介导的防御,提供了额外的证据,生长素促进疾病抑制宿主防御。我们还研究了假设,IAA促进PtoDC 3000毒力通过对病原体的直接影响,并发现IAA调节毒力基因的表达,无论是在文化和植物。因此,除了抑制宿主防御,IAA作为一种微生物信号分子,调节细菌毒力基因的表达。
Modification of host hormone biology is a common strategy used by plant pathogens to promote disease. For example, the bacterial pathogen strain Pseudomonas syringae DC3000 (PtoDC3000) produces the plant hormone auxin (indole-3-acetic acid [IAA]) to promote PtoDC3000 growth in plant tissue. Previous studies suggest that auxin may promote PtoDC3000 pathogenesis through multiple mechanisms, including both suppression of salicylic acid (SA)-mediated host defenses and via an unknown mechanism that appears to be independent of SA. To test if host auxin signaling is important during pathogenesis, we took advantage of Arabidopsis thaliana lines impaired in either auxin signaling or perception. We found that disruption of auxin signaling in plants expressing an inducible dominant axr2–1 mutation resulted in decreased bacterial growth and that this phenotype was suppressed by introducing the sid2–2 mutation, which impairs SA synthesis. Thus, host auxin signaling is required for normal susceptibility to PtoDC3000 and is involved in suppressing SA-mediated defenses. Unexpectedly, tir1 afb1 afb4 afb5 quadruple-mutant plants lacking four of the six known auxin coreceptors that exhibit decreased auxin perception, supported increased levels of bacterial growth. This mutant exhibited elevated IAA levels and reduced SA-mediated defenses, providing additional evidence that auxin promotes disease by suppressing host defense. We also investigated the hypothesis that IAA promotes PtoDC3000 virulence through a direct effect on the pathogen and found that IAA modulates expression of virulence genes, both in culture and in planta. Thus, in addition to suppressing host defenses, IAA acts as a microbial signaling molecule that regulates bacterial virulence gene expression.