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A pair of receptor‐like kinases is responsible for natural variation in shoot growth response to mannitol treatment in A rabidopsis thaliana
Author(s) -
Trontin Charlotte,
Kiani Seifollah,
Corwin Jason A.,
Hématy Kian,
Yansouni Jennifer,
Kliebenstein Dan J.,
Loudet Olivier
Publication year - 2014
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/tpj.12454
Subject(s) - biology , quantitative trait locus , mannitol , gene , arabidopsis thaliana , genetics , phenotype , allele , arabidopsis , locus (genetics) , kinase , candidate gene , microbiology and biotechnology , mutant , biochemistry
Summary 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 A rabidopsis thaliana accessions. Cloning of a major QTL specific to mannitol‐induced stress condition led to identification of EGM 1 and EGM 2 , 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 EGM2 [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 A. thaliana , a species that does not synthesize mannitol. Our findings suggest that the receptor‐like kinases encoded by EGM genes may be activated by mannitol produced by pathogens such as fungi, and may contribute to plant defense responses whenever mannitol is present.