Department of Biology, Washington University, St. Louis, MO, U.S.A.
Division of Biological Sciences, Section of Cell & Developmental Biology, University California San Diego, San Diego, CA, U.S.A.
Mol Plant Microbe Interact. 2020 Aug;33(8):1059-1071. doi: 10.1094/MPMI-02-20-0047-R. Epub 2020 Jun 29.
Modification of host hormone biology is a common strategy used by plant pathogens to promote disease. For example, the bacterial pathogen strain 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 lines impaired in either auxin signaling or perception. We found that disruption of auxin signaling in plants expressing an inducible dominant mutation resulted in decreased bacterial growth and that this phenotype was suppressed by introducing the 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, 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.
宿主激素生物学的修饰是植物病原体用来促进疾病的常见策略。例如，细菌病原体菌株 DC3000（PtoDC3000）产生植物激素生长素（吲哚-3-乙酸[IAA]），以促进 PtoDC3000 在植物组织中的生长。先前的研究表明，生长素可能通过多种机制促进 PtoDC3000 的发病机制，包括抑制水杨酸（SA）介导的宿主防御和通过一种似乎独立于 SA 的未知机制。为了测试宿主生长素信号传导在发病机制中的重要性，我们利用在生长素信号传导或感知中受损的 品系。我们发现，在表达可诱导显性 突变体的植物中破坏生长素信号传导会导致细菌生长减少，并且该表型被引入 突变体抑制，该突变体抑制 SA 合成。因此，宿主生长素信号传导对于对 PtoDC3000 的正常易感性是必需的，并且参与抑制 SA 介导的防御。出乎意料的是，缺乏六个已知生长素核心受体中的四个的四倍体突变体植物，表现出生长素感知降低，支持了更高水平的细菌生长。该突变体表现出升高的 IAA 水平和降低的 SA 介导的防御，提供了生长素通过抑制宿主防御促进疾病的额外证据。我们还研究了 IAA 通过直接作用于病原体促进 PtoDC3000 毒力的假设，并发现 IAA 调节毒力基因的表达，无论是在培养物中还是在植物体内。因此，除了抑制宿主防御外，IAA 还作为一种微生物信号分子，调节细菌毒力基因的表达。
