Stress Tolerance and Glucose Insensitive Phenotypes in Arabidopsis Overexpressing the CpMYB10 Transcription Factor Gene1
Stress Tolerance and Glucose Insensitive Phenotypes in Arabidopsis Overexpressing the CpMYB10 Transcription Factor Gene1
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DOI：
10.1104/pp.103.034199
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发表时间：
2004-05
期刊：
影响因子：
7.4
通讯作者：
M. Villalobos;D. Bartels;G. Iturriaga
中科院分区：
文献类型：
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作者：
M. Villalobos;D. Bartels;G. Iturriaga
复活植物Craterostigma plantagineum有能力在完全脱水的情况下存活。为了进一步了解这种植物的脱水耐性，CpMYB 10转录因子基因的功能特征。CpMYB 10在叶片和根中被脱水和脱落酸（阿坝）处理快速诱导，但在完全水合的组织中没有检测到表达。电泳迁移率变动分析实验显示rCpMYB 10与莱亚Cp 11 -24和CpMYB 10启动子内的特异性mybRE元件结合。CpMYB 10转录本的原位逆转录-PCR反应的本地化表明，响应阿坝在叶片和根的维管组织，薄壁组织和表皮中的表达。将CpMYB 10启动子与GUS基因融合，转化拟南芥，在阿坝和逆境胁迫条件下，拟南芥的多个器官中均有报告基因的表达。CpMYB 10 cDNA在拟南芥中的过量表达导致转基因株系的耐干旱和耐盐性。有趣的是，发现过表达CpMYB 10的植物表现出葡萄糖不敏感和阿坝超敏感的表型。因此，我们的研究结果表明，CpMYB 10在拟南芥介导的胁迫耐受性和改变阿坝和葡萄糖信号反应。
The resurrection plant Craterostigma plantagineum has the ability to survive complete dehydration. In an attempt to further understand desiccation tolerance in this plant, the CpMYB10 transcription factor gene was functionally characterized. CpMYB10 is rapidly induced by dehydration and abscisic acid (ABA) treatments in leaves and roots, but no expression was detected in fully hydrated tissues. Electrophoretic mobility shift assay experiments showed binding of rCpMYB10 to specific mybRE elements within the LEA Cp11-24 and CpMYB10 promoters. Localization of CpMYB10 transcript by in situ reverse transcription-PCR reactions showed expression in vascular tissues, parenchyma, and epidermis both in leaves and roots in response to ABA. Transgenic Arabidopsis plants transformed with CpMYB10 promoter fused to GUS gene showed reporter expression under ABA and stress conditions in several organs. Overexpression of CpMYB10 cDNA in Arabidopsis led to desiccation and salt tolerance of transgenics lines. Interestingly, it was found that plants overexpressing CpMYB10 exhibited Glc-insensitive and ABA hypersensitive phenotypes. Therefore, our results indicate that CpMYB10 in Arabidopsis is mediating stress tolerance and altering ABA and Glc signaling responses.