The Arabidopsis SUMO E3 ligase SIZ1 mediates the temperature dependent trade-off between plant immunity and growth

• Published in: PLoS genetics Vol. 14; no. 1; p. e1007157
• Main Authors: Hammoudi, Valentin, Fokkens, Like, Beerens, Bas, Vlachakis, Georgios, Chatterjee, Sayantani, Arroyo-Mateos, Manuel, Wackers, Paul F. K., Jonker, Martijs J., van den Burg, Harrold A.
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 22.01.2018; Public Library of Science (PLoS)
• Subjects: Acclimatization - genetics; Apoptosis; Arabidopsis; Arabidopsis - genetics; Arabidopsis - growth & development; Arabidopsis - immunology; Arabidopsis Proteins - genetics; Arabidopsis Proteins - physiology; Bioinformatics; Biology and Life Sciences; Body Temperature Regulation - genetics; Cell death; Gene expression; Gene Expression Regulation, Plant; Gene regulation; Genetic aspects; Growth; High temperature; Ligases; Ligases - genetics; Ligases - physiology; Phenotype; Phenotypes; Physiological aspects; Plant immunity; Plant Immunity - genetics; Plant pathology; Plants, Genetically Modified; Proteins; Pseudomonas; Research and Analysis Methods; Rosette; Signal Transduction - genetics; SUMO protein; Temperature; Temperature effects; Thermal properties; Tobacco; Transcription; Ubiquitin-protein ligase; Ubiquitin-Protein Ligases - genetics; Ubiquitin-Protein Ligases - physiology; United States > US; Netherlands
• ISSN: 1553-7404; 1553-7390; 1553-7404
• DOI: 10.1371/journal.pgen.1007157

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.