A pair of receptor‐like kinases is responsible for natural variation in shoot growth response to mannitol treatment in Arabidopsis thaliana. (18th March 2014)

• Record Type: Journal Article
• Authors: Trontin, Charlotte; Kiani, Seifollah; Corwin, Jason A.; Hématy, Kian; Yansouni, Jennifer; Kliebenstein, Dan J.; Loudet, Olivier
• Is Part Of: Plant journal. Volume 78:Number 1(2014:Apr.)
• Page Start: 121
• Page End: 133
• Publication Date: 2014-03-18
• Subjects: Plant molecular biology -- Periodicals; Plant cells and tissues -- Periodicals; Botany -- Periodicals; 580
• DOI: 10.1111/tpj.12454
• Languages: English
• ISSNs: 0960-7412

Abstract

<abstract abstract-type="main" id="tpj12454-abs-0001"> <title>Summary</title> <p>Growth is a complex trait that adapts to the prevailing conditions by integrating many internal and external signals. Understanding the molecular origin of this variation remains a challenging issue. In this study, natural variation of shoot growth under mannitol‐induced stress was analyzed by standard quantitative trait locus mapping methods in a recombinant inbred line population derived from a cross between the Col‐0 and Cvi‐0 <italic>Arabidopsis thaliana</italic> accessions. Cloning of a major QTL specific to mannitol‐induced stress condition led to identification of <italic>EGM1</italic> and <italic>EGM2</italic>, a pair of tandem‐duplicated genes encoding receptor‐like kinases that are potentially involved in signaling of mannitol‐associated stress responses. Using various genetic approaches, we identified two non‐synonymous mutations in the <italic>EGM2</italic>[Cvi] allele that are shared by at least ten accessions from various origins and are probably responsible for a specific tolerance to mannitol. We have shown that the enhanced shoot growth phenotype contributed by the Cvi allele is not linked to generic osmotic properties but instead to a specific chemical property of mannitol itself. This result raises the question of the function of such a gene in <italic>A. thaliana</italic>, a species that does not synthesize mannitol. Our findings suggest that the receptor‐like kinases encoded by <italic>EGM</italic> genes may be activated by mannitol produced by pathogens such as fungi, and may contribute to plant defense responses whenever mannitol is present.</p> </abstract>