Abstract
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.
Highlights
Ambient temperature is a major factor that affects plant growth and development, and plant immunity [1,2]
Multiple examples of high temperature suppression of effector-triggered immunity (ETI) have been described for the TNL-type of immune receptors (Toll Interleukin-1 receptor [TIR], NB-LRR-type) [2], including the tobacco immune receptor N against Tobacco mosaic virus (TMV) [7,8], and resistance mediated by the Arabidopsis immune receptor RPS4, which recognizes the avirulence protein AvrRPS4 from Pseudomonas, is suppressed at high temperature [9]
As snc1-1 auto-immunity is inhibited by PIF4 at high temperature [24], the enhanced immunity of siz1 to PstDC3000 at 28 ̊C might be due to reduced PIF4 function. In line with this notion, we found that siz1 and the sumo1/2KD mutant both showed reduced hypocotyl elongation at 28 ̊C in normal diurnal dark/light cycles (Fig 4A, light; 4B, compare 22C L with 28C L), implying that SIZ1 and the two archetype SUMO proteins, SUMO1 and SUMO2, act as positive regulators of thermomorphogenesis similar to PIF4
Summary
Ambient temperature is a major factor that affects plant growth and development, and plant immunity [1,2]. The tobacco N (Necrosis) gene fails to trigger resistance against Tobacco mosaic virus (TMV) at 30 ̊C, while conferring resistance at 23 ̊C [3]. This is accompanied by the loss of the hypersensitive response (HR) above 27 ̊C. This HR includes a localized cell death that appears to be associated with recognition of pathogen effectors resulting in effector-triggered immunity (ETI) [4,5,6,7]. HR activation by SNC1 required nuclear localization of SNC1, which appeared to be compromised when plants were kept at 28 ̊C [6,7,12]
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