Tsuda Kenichi, Sato Masanao, Glazebrook Jane, Cohen Jerry D, Katagiri Fumiaki
Department of Plant Biology, Microbial and Plant Genomics Institute, University of Minnesota, 1500 Gortner Avenue, St Paul, MN 55108, USA.
Plant J. 2008 Mar;53(5):763-75. doi: 10.1111/j.1365-313X.2007.03369.x. Epub 2007 Nov 14.
Plants respond to pathogen infection using an innate immune system with at least two distinct recognition mechanisms. One mechanism recognizes microbe-associated molecular patterns (MAMPs). The other is based on resistance (R) genes and specifically recognizes certain pathogen virulence factors, including those delivered through the type III secretion system (TTSS) of bacteria. Salicylic acid (SA)-mediated responses are an important part of the R gene-mediated defense. Substantial overlaps between MAMP-triggered and SA-mediated responses have been reported. However, interactions between MAMP-triggered and SA-mediated signaling mechanisms have not been well documented. Here we report intimate interactions between MAMP-triggered and SA-mediated signaling. We found that SA accumulated at a higher level 6 h after treatment with a MAMP, flg22 or inoculation with Pseudomonas syringae pv. tomato DC3000 (PstDC3000) hrcC mutant, which is deficient in TTSS function. Disruptions of SA signaling components, such as SID2 and PAD4, strongly affected MAMP-triggered responses monitored by expression profiling. We found two groups of genes that were induced by PstDC3000 hrcC in an SA-dependent manner. One group was SID2-dependent at all time points, whereas the other was SID2-independent at early time points and SID2-dependent at later time points. Thus, the expression of the latter genes responds to MAMPs through both SA-independent and SA-dependent signaling mechanisms. Strong resistance to PstDC3000 hrcC was dependent on SA signaling. These results indicate that the SA increase triggered by MAMPs is a major component of the MAMP-triggered signaling mechanism, explaining the overlapping spectra of MAMP-triggered and SA-mediated responses.
植物利用具有至少两种不同识别机制的先天免疫系统来应对病原体感染。一种机制识别微生物相关分子模式（MAMPs）。另一种基于抗性（R）基因，专门识别某些病原体毒力因子，包括那些通过细菌的III型分泌系统（TTSS）传递的因子。水杨酸（SA）介导的反应是R基因介导的防御的重要组成部分。据报道，MAMP触发的反应和SA介导的反应之间存在大量重叠。然而，MAMP触发的信号传导机制与SA介导的信号传导机制之间的相互作用尚未得到充分记录。在此，我们报道了MAMP触发的信号传导与SA介导的信号传导之间的密切相互作用。我们发现，在用MAMP、flg22处理或接种丁香假单胞菌番茄致病变种DC3000（PstDC3000）hrcC突变体（其TTSS功能缺陷）6小时后，SA积累到更高水平。SA信号传导成分（如SID2和PAD4）的破坏强烈影响通过表达谱监测的MAMP触发的反应。我们发现两组基因以SA依赖的方式被PstDC3000 hrcC诱导。一组在所有时间点都依赖于SID2，而另一组在早期时间点不依赖于SID2，在后期时间点依赖于SID2。因此，后一组基因的表达通过SA非依赖和SA依赖的信号传导机制对MAMPs作出反应。对PstDC3000 hrcC的强抗性依赖于SA信号传导。这些结果表明，MAMPs触发的SA增加是MAMP触发的信号传导机制的主要组成部分，解释了MAMP触发的反应和SA介导的反应的重叠谱。
