Integrative network-centric approach reveals signaling pathways associated with plant resistance and susceptibility to Pseudomonas syringae
Integrative network-centric approach reveals signaling pathways associated with plant resistance and susceptibility to Pseudomonas syringae
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DOI：
10.1371/journal.pbio.2005956
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发表时间：
2018-12-01
期刊：
影响因子：
9.8
通讯作者：
Popescu, Sorina C.
中科院分区：
文献类型：
--
作者：
Brauer, Elizabeth K.;Popescu, George V.;Popescu, Sorina C.
植物蛋白激酶形成冗余的信号通路来感知微生物病原体并激活免疫。细菌病原体通过分泌效应物来抑制细胞免疫应答，其中一些效应物结合并抑制多种宿主激酶。为了了解细菌效应物如何广泛地结合蛋白激酶以及这些激酶相互作用物的功能，我们首先使用假单胞菌pv.番茄-番茄致病系统我们测试了5个单独的效应子（HopAI 1，AvrPto，HopA 1，HopM 1和HopAF 1）和番茄细胞中的279种番茄激酶之间的相互作用。超过一半的测试激酶与至少一种效应物相互作用，这些激酶中有48%与三种以上的效应物相互作用，这表明在防御中的作用。接下来，我们描述了选择的多效应相互作用激酶的作用，并揭示了它们在基础抵抗、效应触发免疫（ETI）或程序性细胞死亡（PCD）中的作用。这些激酶中的几种的免疫功能仅在效应物存在下才能检测到，这表明当特定细胞功能受到干扰或其作用通常被掩盖时，这些激酶是至关重要的。为了可视化细胞反应背后的激酶网络，我们导出了信号特异性网络。网络的比较揭示了ETI和基础免疫网络之间的有限重叠。此外，当暴露于一些效应物时，基础免疫网络的复杂性增加。该网络被用于成功预测一组新的激酶在基础免疫中的作用。我们的工作表明了更大的基于激酶的防御网络的复杂性，并展示了毒力和非毒力相关的细菌效应子如何改变防御网络的各个部分。
Plant protein kinases form redundant signaling pathways to perceive microbial pathogens and activate immunity. Bacterial pathogens repress cellular immune responses by secreting effectors, some of which bind and inhibit multiple host kinases. To understand how broadly bacterial effectors may bind protein kinases and the function of these kinase interactors, we first tested kinase-effector (K-E) interactions using the Pseudomonas syringae pv. tomato-tomato pathosystem. We tested interactions between five individual effectors (HopAI1, AvrPto, HopA1, HopM1, and HopAF1) and 279 tomato kinases in tomato cells. Over half of the tested kinases interacted with at least one effector, and 48% of these kinases interacted with more than three effectors, suggesting a role in the defense. Next, we characterized the role of select multi-effector-interacting kinases and revealed their roles in basal resistance, effector-triggered immunity (ETI), or programmed cell death (PCD). The immune function of several of these kinases was only detectable in the presence of effectors, suggesting that these kinases are critical when particular cell functions are perturbed or that their role is typically masked. To visualize the kinase networks underlying the cellular responses, we derived signal-specific networks. A comparison of the networks revealed a limited overlap between ETI and basal immunity networks. In addition, the basal immune network complexity increased when exposed to some of the effectors. The networks were used to successfully predict the role of a new set of kinases in basal immunity. Our work indicates the complexity of the larger kinase-based defense network and demonstrates how virulence- and avirulence-associated bacterial effectors alter sectors of the defense network.