详细信息
Characterization of CbCAX51, a Cold Responsive Ca2+/H+ Exchanger from Capsella bursa-pastoris Modulating Cold Tolerance in Plants ( SCI-EXPANDED收录) 被引量:3
文献类型:期刊文献
英文题名:Characterization of CbCAX51, a Cold Responsive Ca2+/H+ Exchanger from Capsella bursa-pastoris Modulating Cold Tolerance in Plants
作者:Li, Weiwei[1] Zhou, Mingqi[1] Zheng, Ye[1] Lin, Ping[2] Yao, Xiaohua[2] Lin, Juan[1]
第一作者:Li, Weiwei
通信作者:Lin, J[1]
机构:[1]Fudan Univ, Sch Life Sci, Inst Plant Biol, Shanghai 200433, Peoples R China;[2]Chinese Acad Forestry, Res Inst Subtrop Forestry, Fuyang 311400, Zhejiang, Peoples R China
年份:2017
卷号:19
期号:4
起止页码:817-824
外文期刊名:INTERNATIONAL JOURNAL OF AGRICULTURE AND BIOLOGY
收录:;WOS:【SCI-EXPANDED(收录号:WOS:000408942100032)】;
基金:This study was supported by the Natural Science Foundation of China (31370346).
语种:英文
外文关键词:Capsella bursa-pastoris; CbCAX51; Ca2+/H+ exchanger; Cold inducible gene; Cold tolerance
摘要:The CV( (Calcium Exchanger) genes constitute a set of signal transductors that are important for plant growth and adaptation to environmental stresses, especially to low temperature. CbC4X51, a Ca2+/H+ exchanger was cloned form Capsella bursa-pastoris, has been reported as a cold inducible gene. Here we showed that the transcriptional level of CbC4X51 in leaf and stem was higher than that in roots. Transcript of CbCAX51 was continuously up-regulated by Ca2+ and Cu2+, and transiently up-regulated by Zn2+ and Li2+, cold stress. GA and ABA. The CbCAX51 protein was predicted to be localized in vacuolar by PSORT to Plant-mPLos, which was further confirmed by the subcellular detection of CbCAX51-GFP fusion protein. When CbCAX51 was transformed into the cold-sensitive plant tobacco, it conferred cold tolerance in tobacco seedlings based on physiological studies. Likewise, overexpression of CbCAX51 can activated some cold responsive genes in transgenic tobacco. Taken together, CbCAX51 is involved in the cold signal transduction and modulation of downstream components to enhance cold tolerance in tobacco. (C) 2017 Friends Science Publishers
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