赤霉素调控硼诱导超表达AtTIP5;1拟南芥下胚轴伸长的分子机制

Gibberellin (GA) can stimulate the hypocotyl elongation by overcoming DELLA-mediated restraint of the transcription factors in Arabidopsis, yet the detailed mechanism remains unclear. We have reported that overexpression of AtTIP5;1 significantly stimulated hypocotyl elongation in Arabidopsis. Further investigation demonstrated that the phytohormone GA was involved in this hypocotyl elongation process. Application of paclobutrazol (PAC, a gibberellin biosynthesis inhibitor) impaired the effects of boron on hypocotyl elongation, indicating endogenous GA are required for boron-induced hypocotyl elongation. Based on the above observations, we suggested that GA may control the boron-induced hypocotyl elongation process through the regulation of AtTIP5;1 expression, and thus has been concluded by us as the boron-GA-DELLA-？-AtTIP5;1-hypocotyl elongation pathway. To further confirm this assumption, in this project, the relationship of boron, gibberellin and AtTIP5;1 was planed to be researched from cellular and molecular levels used the Arabidopsis wild-type, the GA synthesis deficient mutant, the GA insensitive mutant and the corresponding AtTIP5;1 overexpressed transgenic Arabidopsis as the materials. These study will help to clarify the signal transduction pathways of hypocotyl elongation regulated by GA and boron, and will also help us to further understand the detail roles of aquaporins in boron nutrition, and may finally provide a new theoretical foundation of molecular mechanisms of boron and GA in plant growth and development.

赤霉素（GA）可以通过消除DELLA蛋白对PIF3/PIF4转录因子的抑制而促进下胚轴伸长，但具体作用机制仍不清楚。我们研究发现超表达AtTIP5;1拟南芥在硼处理时下胚轴显著伸长，该表型被GA合成抑制剂明显削弱，表明GA是硼诱导超表达AtTIP5;1拟南芥下胚轴伸长的关键因素。基于上述科学发现，我们认为GA是通过调控AtTIP5;1的表达或间接影响活性参与硼诱导下胚轴伸长的过程。本项目以野生型、GA合成缺陷及不敏感突变体、AtTIP5;1突变体以及对应的超表达AtTIP5;1拟南芥为材料，从细胞、分子生物学角度对硼处理时AtTIP5;1、GA和硼在下胚轴伸长过程中的相互关系进行研究，以证明存在硼→GA→DELLA→？→AtTIP5;1→下胚轴伸长这一调控通路，完善GA与硼调控下胚轴伸长的信号传导途径，为深入认识水孔蛋白在硼营养中的作用及硼与GA在植物生长发育中的调控规律提供新的理论基础。

赤霉素（GA）可以通过消除DELLA蛋白对PIF3/PIF4转录因子的抑制而促进下胚轴伸长，但具体作用机制仍不清楚。我们研究发现超表达AtTIP5;1拟南芥在硼处理时下胚轴显著伸长，该表型被GA合成抑制剂明显削弱，表明GA是硼诱导超表达AtTIP5;1拟南芥下胚轴伸长的关键因素。利用数字基因表达谱分析了高硼胁迫下超表达株系与野生型的差异基因。进一步对赤霉素合成及信号转导相关基因进行了定量PCR分析。通过显微观察发现超表达株系下胚轴伸长主要表现为中上部细胞的伸长。而AtTIP5;1两个T-DNA插入的突变体下胚轴中上部细胞的伸长生长不被赤霉素诱导。研究结果表明AtTIP5;1为赤霉素促进下胚轴细胞伸长的关键功能基因。