The Arabidopsis SUMO E3 ligase SIZ1 mediates the temperature dependent trade-off between plant immunity and growth.
The Arabidopsis SUMO E3 ligase SIZ1 mediates the temperature dependent trade-off between plant immunity and growth.
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DOI：
10.1371/journal.pgen.1007157
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发表时间：
2018-01
期刊：
影响因子：
4.5
通讯作者：
van den Burg HA
中科院分区：
文献类型：
--
作者：
Hammoudi V;Fokkens L;Beerens B;Vlachakis G;Chatterjee S;Arroyo-Mateos M;Wackers PFK;Jonker MJ;van den Burg HA
环境温度升高对植物免疫包括自身免疫具有抑制作用。例如，SNC 1依赖性自身免疫在28°C下被完全抑制。我们发现拟南芥类小泛素化突变体siz 1在22°C和28°C下都显示出SNC 1依赖性自身免疫，这在两种温度下都是EDS 1依赖性的。这种siz 1自身免疫表型在两种温度下都增强了对假单胞菌的抗性。此外，siz 1的玫瑰花结大小在28°C下仅微弱恢复，而该温度完全挽救了其他SNC 1依赖性自身免疫突变体的生长缺陷。siz 1的这种热不敏感性与受损的热敏生长反应相关，这与免疫调节剂PAD 4或SNC 1无关。我们的数据表明，这种高温诱导的生长反应强烈依赖于COP 1，而SIZ 1控制这种生长反应的幅度。后一种观点得到了转录组学数据的支持，即SIZ 1控制高温转录变化的幅度和时间，包括PIF 4/BZR 1基因靶标的子集。结合我们的数据表明，SIZ 1抑制SNC 1依赖的电阻响应在正常和高温。与此同时，SIZ 1可能通过COP 1以及PIF 4和BRZ 1的基因调控上游放大黑暗和高温生长反应。环境温度是植物免疫和生长调节的主要因素。最重要的是，高温（>27°C）会阻碍植物的防御反应。高温还通过诱导伸长生长来改变植物形态，这有利于植物“冷却”。这个过程被称为热形态发生。重要的是，SUMO E3连接酶SIZ 1在正常条件下（22°C）抑制植物免疫，但其在高温下的免疫作用尚不清楚。SIZ 1最近被证明sumoylate和激活泛素E3连接酶COP 1，这是热形态发生中的关键参与者，影响该过程的关键转录因子（PIF 4和HY 5）的积累和/或稳定性。在高温下，PIF 4抑制snc 1 -1突变体的SNC 1依赖性生长缺陷和自身免疫。我们报告说，SNC 1依赖性自身免疫反应的一部分被保留和激活的siz 1突变体在高温下导致增强的耐假单胞菌。此外，我们发现SIZ 1控制热形态发生反应，并影响PIF 4和BZR 1基因靶点在高温下的大量表达。我们的数据暗示SIZ 1作用于PIF 4/BZR 1枢纽的上游。结合这些数据，SIZ 1在SNC 1依赖性免疫和高温下生长之间的权衡中具有双重作用，后者可能通过COP 1运行。
Increased ambient temperature is inhibitory to plant immunity including auto-immunity. SNC1-dependent auto-immunity is, for example, fully suppressed at 28°C. We found that the Arabidopsis sumoylation mutant siz1 displays SNC1-dependent auto-immunity at 22°C but also at 28°C, which was EDS1 dependent at both temperatures. This siz1 auto-immune phenotype provided enhanced resistance to Pseudomonas at both temperatures. Moreover, the rosette size of siz1 recovered only weakly at 28°C, while this temperature fully rescues the growth defects of other SNC1-dependent auto-immune mutants. This thermo-insensitivity of siz1 correlated with a compromised thermosensory growth response, which was independent of the immune regulators PAD4 or SNC1. Our data reveal that this high temperature induced growth response strongly depends on COP1, while SIZ1 controls the amplitude of this growth response. This latter notion is supported by transcriptomics data, i.e. SIZ1 controls the amplitude and timing of high temperature transcriptional changes including a subset of the PIF4/BZR1 gene targets. Combined our data signify that SIZ1 suppresses an SNC1-dependent resistance response at both normal and high temperatures. At the same time, SIZ1 amplifies the dark and high temperature growth response, likely via COP1 and upstream of gene regulation by PIF4 and BRZ1. Ambient temperature is a major actor in plant immunity and in growth regulation. Foremost, high temperature (>27°C) is known to block plant defence responses. High temperature also alters the plant morphology by inducing elongation growth, which facilitates plant ‘cooling’. This process is called thermomorphogenesis. Importantly, the SUMO E3 ligase SIZ1 suppresses plant immunity at normal conditions (22°C), but its role in immunity at high temperature was unknown. SIZ1 was recently shown to sumoylate and activate the ubiquitin E3 ligase COP1, a key player in thermomorphogenesis affecting the accumulation and/or stability of key transcription factors for this process (PIF4 and HY5). At high temperature PIF4 suppresses SNC1-dependent growth defects and auto-immunity for the snc1-1 mutant. We report that part of the SNC1-dependent auto-immune response is retained and activated in the siz1 mutant at high temperature resulting in enhanced resistance to Pseudomonas. In addition, we find that SIZ1 controls the thermomorphogenesis response and it affects expression of a substantial subset of PIF4 and BZR1 gene targets in response to high temperature. Our data imply that SIZ1 acts upstream of the PIF4/BZR1 hub. Combined the data highlight that SIZ1 has a dual role in the trade-off between SNC1-dependent immunity and growth at elevated temperature, where the latter aspect potentially runs via COP1.
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影响因子：
6.7
作者：
García AV;Blanvillain-Baufumé S;Huibers RP;Wiermer M;Li G;Gobbato E;Rietz S;Parker JE
通讯作者：
Parker JE
影响因子：
5.6
作者：
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通讯作者：
Parker JE
影响因子：
56.9
作者：
DELANEY, TP;UKNES, S;RYALS, J
通讯作者：
RYALS, J
影响因子：
7.4
作者：
Cheong, Mi Sun;Park, Hyeong Cheol;Yun, Dae-Jin
通讯作者：
Yun, Dae-Jin
影响因子：
7.2
作者：
Erickson, FL;Holzberg, S;Baker, B
通讯作者：
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