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Overexpression of BAK1 causes salicylic acid accumulation and deregulation of cell death control genes

Authors
Kim, Sun YoungShang, YunJoo, Se-HwanKim, Seong-KiNam, Kyoung Hee
Issue Date
Mar-2017
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
BAK1-Overexpression; Cell death; Growth; Salicylic acid; Defense response
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.484, no.4, pp 781 - 786
Pages
6
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume
484
Number
4
Start Page
781
End Page
786
URI
https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/8646
DOI
10.1016/j.bbrc.2017.01.166
ISSN
0006-291X
1090-2104
Abstract
Since the BRI1-Associated Receptor Kinase 1 (BAK1) was firstly identified as a co-receptor of BRI1 that mediates brassinosteroids (BR) signaling, the functional roles of BAKI, as a versatile co-receptor for various ligand-binding leucine-rich repeat (LRR)-containing receptor-like kinase (RLKs), are being extended to involvement with plant immunity, cell death, stomatal development and ABA signaling in plants. During more than a decade of research on the SAKI, it has been known that transgenic Arabidopsis plants overexpressing BAK1 tagged with various reporters do not fully represent its natural functions. Therefore, in this study, we characterized the transgenic plants in which native BAK1 is overexpressed driven by its own promoter. We found that those transgenic plants were more sensitive to BR signaling but showed reduced growth patterns accompanied with spontaneous cell death features that are different from those seen in BR-related mutants. We demonstrated that more salicylic acid (SA) and hydrogen peroxide were accumulated and that expressions of the genes that are known to regulate cell death, such as BONs, BIRs, and SOBIR, were increased in the BAK1-overexpressing transgenic plants. These results suggest that pleiotropic phenotypic alterations shown in the BAK1-overexpressing transgenic plants result from the constitutive activation of SA-mediated defense responses. (C) 2017 Elsevier Inc. All rights reserved.
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