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Arabidopsis ZED1-related kinases mediate temperature-sensitive intersection of immune response and growth homeostasis

ABSTRACT: The rationale: Activation of the immune response antagonizes plant growth and development in absence of pathogen, and such autoimmune phenotype is often suppressed by the elevation of ambient temperature. However, the molecular regulation of ambient temperature-sensitive intersection of immune response and growth is largely elusive. Methods: A genetic screen identified an Arabidopsis mutant, zed1-D, by its high temperature-dependent growth retardation. A combination of molecular, cytological and genetic approaches was used to investigate the molecular basis behind the temperature-sensitive growth and immune response in zed1-D. Key results: A dominant mutation in HOPZ-ETI-DEFICIENT 1 (ZED1) is responsible for a high temperature-dependent autoimmunity and growth retardation in the zed1-D. The autoimmune phenotype in the zed1-D is dependent on the HOPZ-ACTIVATED RESISTANCE 1 (ZAR1). ZED1 and some ZED1-related kinases (ZRKs) are induced by elevated temperature and function cooperatively to suppress the immune response by modulating the transcription of SUPPRESSOR OF NPR1-1 CONSTITUTIVE 1 (SNC1) in absence of pathogen. Main conclusion: Our data reveal a previously unidentified role of ZRKs in ambient temperature-sensitive immune response in absence of pathogen, and thus disclose a possible molecular mechanism underlying temperature-mediated intersection of immune response and growth in plants.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE95665 | GEO | 2018/03/26

REPOSITORIES: GEO

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Project description:Gould2011 - Temperature Sensitive Circadian Clock This model is a temperature sensitive version of Pokhilko et al. 2010 (PMID: 20865009), which is BIOMD0000000273 in BioModels. This model is described in the article: Network balance via CRY signalling controls the Arabidopsis circadian clock over ambient temperatures. Gould PD, Ugarte N, Domijan M, Costa M, Foreman J, Macgregor D, Rose K, Griffiths J, Millar AJ, Finkenstädt B, Penfield S, Rand DA, Halliday KJ, Hall AJ. Mol. Syst. Biol. 2013; 9: 650 Abstract: Circadian clocks exhibit 'temperature compensation', meaning that they show only small changes in period over a broad temperature range. Several clock genes have been implicated in the temperature-dependent control of period in Arabidopsis. We show that blue light is essential for this, suggesting that the effects of light and temperature interact or converge upon common targets in the circadian clock. Our data demonstrate that two cryptochrome photoreceptors differentially control circadian period and sustain rhythmicity across the physiological temperature range. In order to test the hypothesis that the targets of light regulation are sufficient to mediate temperature compensation, we constructed a temperature-compensated clock model by adding passive temperature effects into only the light-sensitive processes in the model. Remarkably, this model was not only capable of full temperature compensation and consistent with mRNA profiles across a temperature range, but also predicted the temperature-dependent change in the level of LATE ELONGATED HYPOCOTYL, a key clock protein. Our analysis provides a systems-level understanding of period control in the plant circadian oscillator. This model is hosted on BioModels Database and identified by: BIOMD0000000564. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

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Arabidopsis ZED1-related kinases mediate temperature-sensitive intersection of immune response and growth homeostasis

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