核质转运受体（NTR）介导的蛋白质核质转运是真核生物信号调节的重要机制之一，并以此响应外界生物或非生物胁迫作用。利用正向遗传学技术，我们前期鉴定了一个干旱敏感突变体xpo1a-4, XPO1A是细胞核输出蛋白受体，但其参与干旱胁迫的作用机理尚不清楚。通过蛋白质免疫共沉淀-质谱分析和酵母双杂交实验，筛选到一个XPO1A互作底物蛋白DCAF2。本项目将在此基础上继续探讨：1）XPO1A与DCAF2互作验证及互作位点分析；2）XPO1A与DCAF2互作对DCAF2核质分布的影响；3）DCAF2响应逆境胁迫分析及其与XPO1A的关系；4）XPO1A与DCAF2互作响应干旱胁迫的机理。重点是解析XPO1A-DCAF2-ABI5的信号级联过程，探明此过程不仅可以阐明XPO1A响应干旱胁迫的作用机制，而且对揭示核质转运在ABA信号转导中的调节功能有重要的启示作用。

Nucleocytoplasmic trafficking of proteins mediated by nuclear transport receptor (NTR) is one of the important signal transduction cascades in Eukaryotes, which helping to adapt to the exogenous environmental factors, biotic and abiotic stresses. In previous study, we identified a hypersensitive mutant, xpo1a-4, to drought stress, XPO1A has been reported to be a nuclear export receptor,while the molecular mechanism of XPO1A involved in drought stress remains unknown. We have screened a interactive protein DCAF2 with XPO1A protein using co-immunoprecipitation/mass- spectrography (IP/MS) and yeast two hybrid methods. In this project, we will focus on: 1) Confirmation of the interaction between XPO1A and DCAF2 and identification of the interactive protein sites; 2) the effection of the interaction between XPO1A and DCAF2 on the nucleocytoplasmic distribution of DACF2 protein; 3) analysis of the DCAF2 gene responding to the abiotic stress and its relation to XPO1A gene; 4) the mechanism of the interaction of XPO1A and DCAF2 responses to drought stress. The emphasis of the project is to illustrate the signal cascade XPO1A-DCAF2-ABI5, which will help not only to understand the molecular mechanism of XPO1A responses to drought stress in Arabidopsis, but also to reveal the roles of nucleocytoplasmic trafficking in regulating ABA signaling.