The Arabidopsis resistance-like gene SNC1 is activated by mutations in SRFR1 and contributes to resistance to the bacterial effector AvrRps4.
The Arabidopsis resistance-like gene SNC1 is activated by mutations in SRFR1 and contributes to resistance to the bacterial effector AvrRps4.
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DOI：
10.1371/journal.ppat.1001172
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发表时间：
2010-11-04
期刊：
影响因子：
6.7
通讯作者：
Gassmann W
中科院分区：
文献类型：
--
作者：
Kim SH;Gao F;Bhattacharjee S;Adiasor JA;Nam JC;Gassmann W
rps 4-RLD 1（SRFR 1）基因的供应者是基于在天然易感的拟南芥属登记RLD中增强的AvrRps 4触发的抗性来鉴定的。没有记录到其他表型效应，SRFR 1参与调节效应子触发的免疫的程度尚不清楚。在这里，我们表明，SRFR 1的突变在登记哥伦比亚-0（Col-0）导致严重的发育迟缓和组成型表达的防御基因PR 1。这些表型是温度依赖性的。srfr 1 -1（RLD背景）和srfr 1 -4（Col-0）之间的杂交表明，矮化是由Col-0中的隐性位点引起的。定位和定向杂交鉴定出Col-0特异性抗性基因SNC 1是导致发育迟缓的基因座。SRFR 1被认为是一种转录抑制因子，SNC 1确实在srfr 1 -4中过表达。有趣的是，SNC 1簇中的共调节基因在srfr 1 -4 snc 1 -11双突变体中也上调，表明SNC 1的过表达不是组成性防御激活的继发效应。此外，Col-0 RPS 4突变体在24°C下而不是在22°C下显示出对表达avrRps 4的细菌的完全易感性，而RLD易感性不是温度依赖性的。rps 4 -2 snc 1 -11双突变体在22°C下表现出增加的但不是完全的易感性，表明抗性途径之间可能存在额外的串扰。有趣的是，当在本氏烟草中瞬时表达时，SRFR 1、RPS 4和SNC 1在细胞质微粒体区室中处于共同的蛋白质复合物中。我们的研究结果突出了SRFR 1作为一个收敛点，在至少一个子集的TIR-NBS-LRR蛋白介导的免疫拟南芥。基于从我们的研究结果中明显的串扰，他们还建议Col-0中的组成性抗性表型的报告需要考虑SNC 1的可能参与。植物和人类一样，有一个免疫系统来抵御疾病。这种免疫系统通过检测非植物分子和蛋白质来寻找致病微生物和其他入侵者的存在。植物依靠这种监视在正确的时间激活适当强度的抗菌反应;与人类一样，过度活跃的免疫系统可能对植物有害。我们研究植物如何实现适当的平衡，利用遗传学和参考植物拟南芥和细菌性植物病原体假单胞菌之间的相互作用。所谓的植物抗性蛋白是重要的免疫激活剂，其直接或间接地拦截由病原体部署的外源蛋白。抗性蛋白通常被认为是高度特异性的检测器，其仅对单一病原体蛋白做出响应。然而，在研究一种名为SRFR 1的植物免疫负调节因子时，我们发现了不同抗性蛋白之间令人惊讶的串扰水平，这种串扰仅在某些环境条件下（如低温）才变得明显。我们还表明，SRFR 1和这些抗性蛋白相互结合，可能解释了观察到的串扰。因此，我们的工作突出了抗性途径之间的联系，并提供了深入了解植物先天免疫反应的分子结构。
The SUPPRESSOR OF rps4-RLD1 (SRFR1) gene was identified based on enhanced AvrRps4-triggered resistance in the naturally susceptible Arabidopsis accession RLD. No other phenotypic effects were recorded, and the extent of SRFR1 involvement in regulating effector-triggered immunity was unknown. Here we show that mutations in SRFR1 in the accession Columbia-0 (Col-0) lead to severe stunting and constitutive expression of the defense gene PR1. These phenotypes were temperature-dependent. A cross between srfr1-1 (RLD background) and srfr1-4 (Col-0) showed that stunting was caused by a recessive locus in Col-0. Mapping and targeted crosses identified the Col-0-specific resistance gene SNC1 as the locus that causes stunting. SRFR1 was proposed to function as a transcriptional repressor, and SNC1 is indeed overexpressed in srfr1-4. Interestingly, co-regulated genes in the SNC1 cluster are also upregulated in the srfr1-4 snc1-11 double mutant, indicating that the overexpression of SNC1 is not a secondary effect of constitutive defense activation. In addition, a Col-0 RPS4 mutant showed full susceptibility to bacteria expressing avrRps4 at 24°C but not at 22°C, while RLD susceptibility was not temperature-dependent. The rps4-2 snc1-11 double mutant showed increased, but not full, susceptibility at 22°C, indicating that additional cross-talk between resistance pathways may exist. Intriguingly, when transiently expressed in Nicotiana benthamiana, SRFR1, RPS4 and SNC1 are in a common protein complex in a cytoplasmic microsomal compartment. Our results highlight SRFR1 as a convergence point in at least a subset of TIR-NBS-LRR protein-mediated immunity in Arabidopsis. Based on the cross-talk evident from our results, they also suggest that reports of constitutive resistance phenotypes in Col-0 need to consider the possible involvement of SNC1. Plants, like humans, have an immune system to defend against disease. This immune system seeks out the presence of disease-causing microbes and other invaders by detecting non-plant molecules and proteins. Plants rely on this surveillance to activate an antimicrobial response of appropriate strength at the right time; as with humans, an overactive immune system can be harmful to plants. We study how plants achieve an appropriate balance, using genetics and the interaction between the reference plant Arabidopsis thaliana and the bacterial plant pathogen Pseudomonas syringae. So-called plant resistance proteins are important activators of immunity that directly or indirectly intercept foreign proteins deployed by pathogens. Resistance proteins are generally thought to be highly specific detectors that only respond to a single pathogen protein. However, while working with a negative regulator of plant immunity called SRFR1, we discovered a surprising level of cross-talk between different resistance proteins that becomes evident only under certain environmental conditions such as low temperature. We also show that SRFR1 and these resistance proteins bind to each other, possibly explaining the observed cross-talk. Our work thus highlights linkages between resistance pathways and provides insight into the molecular architecture of the plant innate immune response.
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