拟南芥气孔由一对保卫细胞组成。four lip（flp）突变体是最早发现的气孔突变体之一，FLP基因突变导致保卫细胞母细胞冗余分裂，形成异常的多细胞气孔结构。已有结果表明FLP作为MYB转录因子可直接负调控CDKB1;1、CDKA;1、CYCA2;3基因转录，但FLP所参与的气孔发育后期的对称分裂调控机制尚不清楚。我们采用正向遗传学方法对flp-1突变体进行了EMS诱变，从诱变群中筛选到一个可抑制flp-1气孔表型的突变体植株flp-1 fsp1，并完成该基因的图位克隆。转化FSP1能够使flp-1 fsp1的植株重现flp-1气孔表型。fsp1单突变体也表现出保卫细胞母细胞分裂缺陷,表明FSP1参与了FLP所调控的气孔发育后期细胞分裂。我们拟利用分子生物学、生物化学和细胞生物学等技术，对FSP1与FLP及细胞周期蛋白的关系进行解析，期待能进一步揭示气孔发育中对称分裂的精细的分子调控机制。

Arabidopsis four lips (flp-1) is one of the earliest found stomatal mutants. Mutation of FLP gene leads to extra divisions within guard mother cells. As a MYB transcription factor, FLP could directly regulate the transcrition of CDKB1;1,CDKA;1 and CYCA2;3 . However, the molecular mechanism of how FLP regulates the GMC symmtric division at the terminal stage of stomatal development has not been fully discovered. By the means of forward genetic approaches, we isolated a flp-1 fsp1 mutant from the populations of EMS mutagenesis, in which the stomatal defective phenotype of flp-1 was suppressed. We have identified this gene using the map-based cloning. Trasformation of a construct harboring FSP1 was able to reverse the stomatal defects of flp-1 fsp1 plants to that of flp-1 muants. Single mutant of fsp1 exhibits defective divison in guard mother cells, suggesting that FSP1 is involved in FLP-regulated terminal symmetric divison of stomatal development. Using approaches of molecular, biochemical and cellular biology, we will probe the interaction between FSP1, FLP and cell cycle genes. The results for the above study will further enrich our knowledge about the fine regulation of cell symmetric diviosn happened in stomatal development.