蓝光诱导气孔开放的信号转导中，催化蛋白磷酸化的激酶的作用研究得还不是很清楚。本项目前期结果显示：促分裂原活化的蛋白激酶级联中MAPKKKa与MKKb基因（不影响气孔发育）突变后蓝光下气孔开度比野生型小，且两种蛋白之间有相互作用；此外，蓝光受体Phot1与MAPKKKa有相互作用，且可能将MAPKKKa磷酸化。本项目将利用细胞生物学、分子生物学、生物化学等技术进一步研究：（1）MAPKKKa-MKKb在调控气孔开放过程中的磷酸化及上下游关系；（2）确定Phot1能否将MAPKKKa磷酸化，探究磷酸化位点及功能， 以及体外Phot1对 MAPKKKa活性的影响；（3）植物体内Phot1对MAPKKKa活性的影响；从而揭示在蓝光诱导气孔开放过程中可能存在Phot1-MAPKKKa-MKKb这一调节方式。本项目的研究结果将丰富气孔光调控机制，也为利用基因工程技术培育耐旱植物提供有价值的信息。

In the signal network of blue light-induced stomatal opening, the kinases that catalyze the phosphorylation of proteins are not clear. Our premilinary results showed that mutation of MAPKKKa and MKKb genes, which belong to the mitogen-activated protein kinases family and do not affect stomatal developments, led to the reduced stomatal apertures in response to blue light, and MAPKKKa interacted with MKKb. In addition, blue light receptor Phot1 showed interaction with MAPKKKa, and possibly phosphorylated MAPKKKa. In this project, by utilizing cell biological, genetic and biochemical techniques, we will further study: (1) the phosphorylation of MKKb by MAPKKKa, and the up-down stream relationship between MAPKKKa and MKKb during stomatal opening, (2) confirm whether Phot1 phosphorylated MAPKKKa, the possible phosphorylated sites and the biological function of the phosphorylated sites in MAPKKKa, and the effect of Phot1 on the kinse activity of MAPKKKa in vitro; (3) how Phot1 affects the kinase activity of MAPKKKa in plants. The results from this project will reveal a possible regulatory pathway including Phot1-MAPKKKa-MKKb in blue light-induced stomatal opening. The conclusion from this research will enrich signal transduction mechanism in the guard cell during stomatal opening, and will provide useful information for the cultivation of drought-resistant plants with genetic manipulation.