膜泡运输是细胞各项生命活动的基础。我们在前期研究中发现拟南芥MAG2与MIP1,2,3形成拴留复合体，在ER-Golgi逆向运输中调控运输囊泡与内质网的融合[1,2]。这些基因缺失使内质网向外部的运输受阻，造成储藏蛋白质前体不能有效运离而蓄积在内质网中。为了进一步探究MAG2相关的ER-Golgi膜泡运输机制，我们制作了MAG2和同源蛋白MAG2-Like(MAL)的双重突变体，发现其不仅膜泡运输受到更大影响，而且生长发育受到严重抑制，产生矮小、分枝多、根系不发达等表型缺陷，暗示ER-Golgi膜泡运输障碍影响植物生长发育。本项研究计划检测mag2mal的生长素水平和分布以及生长素转运蛋白PIN和PILS的表达量和定位，同时观察双突变体内质网和高尔基体形态和功能变化并评定ER-Dolgi膜泡运输效率。将研究结果有机地结合进行分析，初步揭示膜泡运输与植物生长发育的相关性。

Vesicle transport is the basic of various life activities of cells. In our previous work, we found that Arabidopsis MAG2, MIP1,2 and MIP3 form a tethering complex, regulating fusion of transport vesicle to the ER membrane during ER-Golgi retrograde transport. When these genes are defective, exit from the ER of proteins is blocked, resulting in precursors of storage proteins can not exit and abnormally accumulated in the ER lumen. To further reveal mechanism underlying MAG2-relating ER-Golgi vesicle transport, we made double mutant of MAG2 and its homolog protein-MAG2-Like (MAL). We found that in addition to more serious defects on vesicle transport, mag2mal mutant is defective on growth and development. The plant is dwarf, having shorter roots and more shoot branches. These suggest that defects on ER-Golgi transport affect growth and development of plant. In this project, we plan to detect level and distribution of auxin, and expression and localization of the auxin transporters, PINs and PILSs, in mag2mal. We also plan to observe morphology of the ER and Golgi apparatus and evaluate efficiency of ER-Golgi transport. Combining the results, it is expected to reveal the correlations between ER-Golgi vesicle transport and plant growth and development.