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Abiotic stress‐inducible receptor‐like kinases negatively control ABA signaling in Arabidopsis
Author(s) -
Tanaka Hidenori,
Osakabe Yuriko,
Katsura Shogo,
Mizuno Shinji,
Maruyama Kyonoshin,
Kusakabe Kazuya,
Mizoi Junya,
Shinozaki Kazuo,
YamaguchiShinozaki Kazuko
Publication year - 2012
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.2012.04901.x
Subject(s) - arabidopsis , kinase , microbiology and biotechnology , biology , abiotic stress , protein kinase domain , osmotic shock , signal transduction , mutant , rna interference , gene , biochemistry , rna
Summary Membrane‐anchored receptor‐like protein kinases (RLKs) recognize extracellular signals at the cell surface and activate the downstream signaling pathway by phosphorylating specific target proteins. We analyzed a receptor‐like cytosolic kinase (RLCK) gene, ARCK1 , whose expression was induced by abiotic stress. ARCK1 belongs to the cysteine‐rich repeat (CRR) RLK sub‐family and encodes a cytosolic protein kinase. The arck1 mutant showed higher sensitivity than the wild‐type to ABA and osmotic stress during the post‐germinative growth phase. CRK36, an abiotic stress‐inducible RLK belonging to the CRR RLK sub‐family, was screened as a potential interacting factor with ARCK1 by co‐expression analyses and a yeast two‐hybrid system. CRK36 physically interacted with ARCK1 in plant cells, and the kinase domain of CRK36 phosphorylated ARCK1 in vitro . We generated CRK36 RNAi transgenic plants, and found that transgenic plants with suppressed CRK36 expression showed higher sensitivity than arck1‐2 to ABA and osmotic stress during the post‐germinative growth phase. Microarray analysis using CRK36 RNAi plants revealed that suppression of CRK36 up‐regulates several ABA‐responsive genes, such as LEA genes, oleosin, ABI4 and ABI5 . These results suggest that CRK36 and ARCK1 form a complex and negatively control ABA and osmotic stress signal transduction.