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BAK7 displays unequal genetic redundancy with BAK1 in brassinosteroid signaling and early senescence in arabidopsis

Title
BAK7 displays unequal genetic redundancy with BAK1 in brassinosteroid signaling and early senescence in arabidopsis
Authors
Jeong Y.J.Shang Y.Kim B.H.Kim S.Y.Song J.H.Lee J.S.Lee M.M.Li J.Nam K.H.
Ewha Authors
이준승
SCOPUS Author ID
이준승scopusscopus
Issue Date
2010
Journal Title
Molecules and Cells
ISSN
1016-8478JCR Link
Citation
vol. 29, no. 3, pp. 259 - 266
Indexed
SCI; SCIE; SCOPUS; KCI WOS scopus
Abstract
BRI1-Associated kinase1 (BAK1), a five leucine-rich-repeat containing receptor-like serine/threonine kinase, has been shown to have dual functions: mediating brassinosteroid (BR) signaling and acting in the BR-independent plant defense response. Sequence analysis has revealed that BAK1 has two homologs, BAK7 and BAK8. Because BAK8 deviates from the canonical RD kinase motif, we focused on the functional analysis of BAK7. The expression pattern and tissues in which BAK7 appeared partially overlapped with those observed for BAK1. Expression levels of BAK7 increased in the bak1 mutant. Overexpression of BAK7 rescued the bri1 mutant phenotype, indicating that BAK7 can compensate for BAK1 in BR-mediated processes, especially in the absence of BAK1. However, root and hypocotyl elongation patterns of transgenic plants overexpressing BAK1 or BAK7 appeared to be different from the patterns observed in a BRI1 overexpressor. Furthermore, the sensitivity of transgenic plants overexpressing BAK7 to brassinazole, a biosynthetic inhibitor of brassinolide (BL), did not change compared to that of wild-type plants. In addition, we generated transgenic plants expressing BAK7 RNA interference constructs and found severe growth retardation and early senescence in these lines. Taken together, these results suggest that BAK7 is a component of the BR signaling pathway, with varying degrees of genetic redundancy with BAK1, and that it affects plant growth via BL-independent pathways in vivo. © 2010 KSMCB.
DOI
10.1007/s10059-010-0024-0
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자연과학대학 > 생명과학전공 > Journal papers
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