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向日葵胚胎中热激基因启动子的转录激活:ABI3与热激因子之间的协同作用。

Transcriptional activation of a heat shock gene promoter in sunflower embryos: synergism between ABI3 and heat shock factors.

作者信息

Rojas A, Almoguera C, Jordano J

机构信息

Instituto de Recursos Naturales y Agrobiología, Consejo Superior de Investigaciones Científicas, Apartado 1052, 41080 Sevilla, Spain.

出版信息

Plant J. 1999 Dec;20(5):601-10. doi: 10.1046/j.1365-313x.1999.00635.x.

DOI:10.1046/j.1365-313x.1999.00635.x
PMID:10652132
Abstract

Transient expression analyses in sunflower embryos demonstrated that ABI3, a seed-specific transcription factor from Arabidopsis, activated chimaeric genes with the Ha hsp17.7 G4 promoter. Nucleotide substitutions at crucial positions of heat shock cis-elements established that they are required for the transcriptional activation involving ABI3. Trans-activation with Lp-HSFA1, a heat shock factor from tomato, reproduced the activation patterns of wild-type and mutant promoters observed with ABI3. In addition, ABI3 and Lp-HSFA1 synergistically activated the Ha hsp17. 7 G4 promoter, but only when it contained the intact proximal and distal heat shock cis-elements. The activation domain of Lp-HSFA1 was necessary for promoter activation. An amino terminal deletion of ABI3 had dominant negative effects on activation by Lp-HSFA1. We failed to detect a substantial transcriptional activation by ABI3 in the absence of either functional heat shock factors or heat shock elements (HSEs). Furthermore, the wild-type, but not the mutant HSEs (from - 136 to - 49 in Ha hsp17.7 G4) were sufficient, in the context of a - 46 CaMV 35S promoter, to support activation by Lp-HSFA1, or Lp-HSFA1 and ABI3. These results demonstrate, for the first time, transcriptional activation of a heat shock protein promoter by ABI3. We also suggest that ABI3 functions as a transcriptional co-activator through heat shock factors.

摘要

在向日葵胚胎中的瞬时表达分析表明,来自拟南芥的种子特异性转录因子ABI3可激活带有Ha hsp17.7 G4启动子的嵌合基因。热休克顺式元件关键位置的核苷酸替换表明,它们是ABI3介导的转录激活所必需的。用来自番茄的热休克因子Lp-HSFA1进行反式激活,重现了用ABI3观察到的野生型和突变型启动子的激活模式。此外,ABI3和Lp-HSFA1协同激活Ha hsp17.7 G4启动子,但前提是它包含完整的近端和远端热休克顺式元件。Lp-HSFA1的激活结构域对于启动子激活是必需的。ABI3的氨基末端缺失对Lp-HSFA1的激活具有显性负效应。在缺乏功能性热休克因子或热休克元件(HSEs)的情况下,我们未能检测到ABI3的大量转录激活。此外,在 - 46 CaMV 35S启动子的背景下,野生型而非突变型HSEs(在Ha hsp17.7 G4中从 - 136到 - 49)足以支持Lp-HSFA1或Lp-HSFA1与ABI3的激活。这些结果首次证明了ABI3对热休克蛋白启动子的转录激活作用。我们还表明,ABI3通过热休克因子作为转录共激活因子发挥作用。

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