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Arabidopsis ESK1 encodes a novel regulator of freezing tolerance
Author(s) -
Xin Zhanguo,
Mandaokar Ajin,
Chen Junping,
Last Robert L.,
Browse John
Publication year - 2007
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/j.1365-313x.2006.02994.x
Subject(s) - arabidopsis , biology , gene , abscisic acid , genetics , locus (genetics) , freezing tolerance , regulator , microbiology and biotechnology , transcription factor , gene family , gene expression , mutant
Summary The eskimo1 ( esk1 ) mutation of Arabidopsis resulted in a 5.5°C improvement in freezing tolerance in the absence of cold acclimation. Here we show that the increase in freezing tolerance is not associated with any increase in the ability to survive drought or salt stresses, which are similar to freezing in their induction of cellular dehydration. Genome‐wide comparisons of gene expression between esk1‐1 and wild type indicate that mutations at esk1 result in altered expression of transcription factors and signaling components and of a set of stress‐responsive genes. Interestingly, the list of 312 genes regulated by ESK1 shows greater overlap with sets of genes regulated by salt, osmotic and abscisic acid treatments than with genes regulated by cold acclimation or by the transcription factors CBF3 and ICE1, which have been shown to control genetic pathways for freezing tolerance. Map‐based cloning identified the esk1 locus as At3g55990 . The wild‐type ESK1 gene encodes a 57‐kDa protein and is a member of a large gene family of DUF231 domain proteins whose members encode a total of 45 proteins of unknown function. Our results indicate that ESK1 is a novel negative regulator of cold acclimation. Mutations in the ESK1 gene provide strong freezing tolerance through genetic regulation that is apparently very different from previously described genetic mechanisms of cold acclimation.