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Cited 21 time in webofscience Cited 22 time in scopus
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Ectopic expression of an Arabidopsis dehydration-responsive element-binding factor DREB2C improves salt stress tolerance in crucifers

Authors
Song, ChieunJe, JihyunHong, Joon KiLim, Chae Oh
Issue Date
Aug-2014
Publisher
SPRINGER
Keywords
Arabidopsis; Canola; NaCl stress; Transgenic plant; Transcriptional activator
Citation
PLANT CELL REPORTS, v.33, no.8, pp 1239 - 1254
Pages
16
Indexed
SCI
SCIE
SCOPUS
Journal Title
PLANT CELL REPORTS
Volume
33
Number
8
Start Page
1239
End Page
1254
URI
https://scholarworks.gnu.ac.kr/handle/sw.gnu/18869
DOI
10.1007/s00299-014-1612-9
ISSN
0721-7714
1432-203X
Abstract
DREB2C acts as a transcriptional activator of the salt tolerance-related COLD - REGULATED 15A gene. DEHYDRATION-RESPONSIVE ELEMENT BINDING FACTOR 2C (DREB2C) regulates plant responses to heat stress. We report here that DREB2C is induced by NaCl stress in Arabidopsis, based on quantitative RT-PCR analyses of transcript levels and DREB2C promoter-controlled GUS activity assays. Constitutive overexpression of DREB2C from the cauliflower mosaic virus (CaMV) 35S promoter led to enhanced salt tolerance in transgenic Arabidopsis and canola plants that was characterized by higher chlorophyll content, lower tissue Na+ content, reduced rate of water loss, and tighter membrane integrity in plants grown in NaCl-containing medium. Basal expression of the stress-responsive genes COLD-REGULATED 15A (COR15A), RESPONSIVE TO DEHYDRATION (RD) 29A and RD29B, was higher in transgenic DREB2C-overexpressing Arabidopsis plants than in the wild-type. Promoter transactivation assays and electrophoretic mobility-shift assays showed that DREB2C interacts directly with the three DREs in the COR15A promoter, both in vivo and in vitro. Transgenic Arabidopsis constitutively overexpressing COR15A from the CaMV35S promoter exhibited greater NaCl tolerance than the untransformed wild-type. Taken together, the data suggest that DREB2C functions as transcriptional activator that promotes NaCl tolerance, in part through upregulation of the stress-responsive gene COR15A.
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