Overexpression of an Arabidopsis cysteine-rich receptor-like protein kinase, CRK5, enhances abscisic acid sensitivity and confers drought tolerance

Receptor-like kinases (RLKs) have been reported to regulate many developmental and defense process, but only a few members have been functionally characterized. In the present study, our observations suggest that one of the RLKs, a membrane-localized cysteine-rich receptor-like protein kinase, CRK5,...

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Published in:Journal of experimental botany 2016-09, Vol.67 (17), p.5009-5027
Main Authors: Lu, Kai, Liang, Shan, Wu, Zhen, Bi, Chao, Yu, Yong-Tao, Wang, Xiao-Fang, Zhang, Da-Peng
Format: Article
Language:English
Subjects:
Abscisic Acid - physiology
Arabidopsis - metabolism
Arabidopsis - physiology
Arabidopsis Proteins - physiology
Dehydration - metabolism
Dehydration - physiopathology
Electrophoretic Mobility Shift Assay
Escherichia coli
Nicotiana
Plant Growth Regulators - physiology
Plants, Genetically Modified
Protein Serine-Threonine Kinases - physiology
Real-Time Polymerase Chain Reaction
Receptors, Cell Surface - physiology
RESEARCH PAPER
Two-Hybrid System Techniques
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Summary:Receptor-like kinases (RLKs) have been reported to regulate many developmental and defense process, but only a few members have been functionally characterized. In the present study, our observations suggest that one of the RLKs, a membrane-localized cysteine-rich receptor-like protein kinase, CRK5, is involved in abscisic acid (ABA) signaling in Arabidopsis thaliana. Overexpression of CRK5 increases ABA sensitivity in ABA-induced early seedling growth arrest and promotion of stomatal closure and inhibition of stomatal opening. Interestingly, and importantly, overexpression of CRK5 enhances plant drought tolerance without affecting plant growth at the mature stages and plant productivity. Transgenic lines overexpressing a mutated form of CRK5, CRK5K372E with the change of the 372nd conserved amino acid residue from lysine to glutamic acid in its kinase domain, result in wild-type ABA and drought responses, supporting the role of CRK5 in ABA signaling. The loss-of-function mutation of the CRK5 gene does not affect the ABA response, while overexpression of two homologs of CRK5, CRK4 and CRK19, confers ABA responses, suggesting that these CRK members function redundantly. We further showed that WRKY18, WRKY40 and WRKY60 transcription factors repress the expression of CRK5, and that CRK5 likely functions upstream of ABI2 in ABA signaling. These findings help in understanding the complex ABA signaling network.
ISSN:0022-0957
1460-2431
DOI:10.1093/jxb/erw266