A TIR–NBS protein encoded by Arabidopsis Chilling Sensitive 1 (CHS1) limits chloroplast damage and cell death at low temperature. (22nd May 2013)

• Record Type: Journal Article
• Authors: Zbierzak, Anna Maria; Porfirova, Svetlana; Griebel, Thomas; Melzer, Michael; Parker, Jane E.; Dörmann, Peter
• Is Part Of: Plant journal. Volume 75:Number 4(2013:Aug.)
• Page Start: 539
• Page End: 552
• Publication Date: 2013-05-22
• Subjects: Plant molecular biology -- Periodicals; Plant cells and tissues -- Periodicals; Botany -- Periodicals; 580
• DOI: 10.1111/tpj.12219
• Languages: English
• ISSNs: 0960-7412

Abstract

<abstract abstract-type="main" xml:lang="en" id="tpj12219-abs-0001"> <title>Summary</title> <p>Survival of plants at low temperature depends on mechanisms for limiting physiological damage and maintaining growth. We mapped the <italic>chs1‐1</italic> (<italic>chilling sensitive1‐1</italic>) mutation in Arabidopsis accession Columbia to the TIR‐NBS gene At1g17610. In <italic>chs1‐1</italic>, a single amino acid exchange at the CHS1 N‐terminus close to the conserved TIR domain creates a stable mutant protein that fails to protect leaves against chilling stress. The sequence of another TIR‐NBS gene (At5g40090) named <italic>CHL1</italic> (<italic>CHS1‐like 1</italic>) is related to that of <italic>CHS1</italic>. Over‐expression of <italic>CHS1</italic> or <italic>CHL1</italic> alleviates chilling damage and enhances plant growth at moderate (24°C) and chilling (13°C) temperatures, suggesting a role for both proteins in growth homeostasis. <italic>chs1‐1</italic> mutants show induced salicylic acid production and defense gene expression at 13°C, indicative of autoimmunity. Genetic analysis of <italic>chs1‐1</italic> in combination with defense pathway mutants shows that <italic>chs1‐1</italic> chilling sensitivity requires the TIR‐NBS‐LRR and basal resistance regulators encoded by <italic>EDS1</italic> and <italic>PAD4</italic> but not salicylic acid. By following the timing of metabolic, physiological and chloroplast ultrastructural changes in <italic>chs1‐1</italic> leaves during chilling, we have established that alterations in photosynthetic complexes and thylakoid membrane integrity precede leaf cell death measured by ion leakage. At 24°C, the <italic>chs1‐1</italic> mutant appears normal but produces a massive necrotic response to virulent <italic>Pseudomonas syringae</italic> pv. <italic>tomato</italic> infection, although this does not affect bacterial proliferation. Our results suggest that CHS1 acts at an intersection between temperature sensing and biotic stress pathway activation to maintain plant performance over a range of conditions.</p> </abstract>