脱落酸跨膜转运分子机制的研究

Abscisic acid (ABA) is a phytohormone that plays a critical role in the growth and development as well as stress response in plants. Investigation of the ABA signaling pathway is of great interest to both basic research and potential applications. The molecular mechanism underlying ABA perception and signal transduction has been largely elucidated owing to the rigorous multi-disciplinary studies in the past few years. It was identified that the PYL family proteins are cellular ABA receptors. PYLs, upon ABA binding, undergo conformational changes that result in physical association and inhibition of the phosphatase activities of PP2Cs, an event that relieves PP2Cs-mediated inhibition of the downstream kinases, SnRK2.2/3/6. Subsequently, the auto-phosphorylated SnRK2s activate the transcriptional factors that induce the expression of ABA-responsive genes. Despite the advancement in the understanding of ABA signal transduction, it remains elusive how ABA is efficiently transported across the membrane. ABA is synthesized in the vascular parenchyma cells. It requires efficient transport system to function in different cell types. Since 2010, a number of proteins including ABCG25, ABCG40, and AIT1 have been identified as ABA transporters. According to these studies, ABA can be transported out of the parenchyma cells by ABCG25, and imported into other cells by ABCG40 and AIT1. In order to gain a mechanistic understanding of membrane transport of ABA, we plan to combine structural biology, biochemistry, and bioinformatics to elucidate the structures of one or more of the ABA transporters and elucidate their working mechanisms including substrate selection, conformational changes, and the energy coupling involved in the transport of ABA across lipid bilayer.

脱落酸（abscisic acid，ABA）是调控植物生长发育和应激反应最重要的几种激素之一，对植物的正常生理活动以及对抗逆境具有至关重要的作用。因此，关于ABA代谢与信号传导的研究具有广泛的基础意义和应用价值。研究表明，ABA能够结合受体蛋白PYLs，进而抑制PP2Cs的去磷酸化酶活性，从而解除PP2Cs对SnRKs激酶活性的抑制，引起ABA效应，促进气孔关闭及抑制种子萌芽。然而，ABA是如何被高效地跨膜运输，仍有待研究。自2010年以来的研究发现，ABA可以被ABCG25转运出维管束薄壁细胞，被ABCG40和AIT1转运至细胞内。然而，对于ABCG25、ABCG40和AIT1的研究刚刚起步。对于它们识别ABA的特异性、作用机制、动力来源等还需要进一步研究。我们计划依托于本实验室在膜蛋白结构生物学研究的优势，拟利用结构生物学、生物化学及生物信息学方法，对ABA跨膜转运的机制进行研究。