拟南芥利用种子储存的能源物质维持萌发后幼苗从异养到光合自养过渡，然而种子萌发到成苗如何避开水涝的机制并不清楚。我们前期筛到一个编码ABC转运蛋白基因SDM1，该基因突变导致无糖培养的拟南芥幼苗出现子叶透明、气孔周围无脂肪酸聚集和根生长停滞等现象。外源添加糖或提高培养基硬度，突变体sdm1恢复拟南芥野生型的生长发育表型。上述结果暗示，SDM1可能转运脂肪酸或者脂肪酸前体物质介导疏水性脂肪酸在气孔聚集以防止水大量进入子叶，提高幼苗发育早期抵御水涝能力，该过程受糖特异调节。然而目前糖调控脂肪酸在植物气孔附近聚集抵御水涝的机制并不清楚。本项目拟通过分析ABC转运蛋白SDM1转运底物，探讨蔗糖和葡萄糖特异恢复突变体sdm1表型的机理，解析SDM1上游信号感受和下游底物选择机制，明确脂肪酸气孔定位与植物幼苗发育早期抵御水涝的关系。该研究有望揭示糖调节蛋白SDM1促进脂肪酸在气孔周围定位应答水涝的机制。

Utilization of seed storage reserves is essential for the transformation from heterotrophy to photoautotrophy during seedling establishment after seed germination in Arabidopsis. However, plant how to avoid the flooding in process of seedling establishment is not clear. Here, we have screened a gene SDM1 which encoded an ABC transport protein, and the mutation of SDM1 resulted in a function defect in fatty acid accumulation around guard cell in the absent of exogenous sucrose and aborted the transformation from heterotrophy to photoautotrophy. Interestingly, the defects in fatty acid accumulation around guard cell of sdm1 were restored by adding sucrose to medium. Consistently, the seedling establishment was also restored by adding sucrose to medium or enhancing the hardness of medium. Our data suggested that SDM1 might function as a transporter of some fatty acid or their precursor substance in mediating the hydrophobic fatty acid accumulation around guard cell, so that it could prevent the water invade into the tissue of cotyledons via the stomata and ensure the cotyledon absorb sufficient CO2 from the atmosphere. Sugar may play a vital role in accumulation of hydrophobic fatty acid around guard cell. However, the mechanism of SDM1 in regulating the accumulation of fatty acid around guard cell in response to the waterlogging stress still remains unclear. In this study, we will analyze the transfer substrates of SDM1 and elucidate the relationship between the fatty acid accumulation in guard cell and the waterlogging stress. We will research the effects of SDM1 phosphorylation and to elucidate the mechanism that the sucrose and glucose could rescue the defective phenotype of sdm1 to elucidate the mechanism of upstream signals perception and downstream substrate selection during SDM1 functions. This study may provide clues for understanding the molecular mechanism of SDM1 in regulating fatty acid location on guard cells in response to the waterlogging stress.