多细胞生物的发育由细胞分裂和分化过程完美协调。这种协调是如何获得的，以及发育调节因子如何作用细胞周期中枢组件(如E2F)的分子机制是生物学研究的关键问题。拟南芥气孔由一个保卫母细胞经一次对称分裂形成的两个保卫细胞围成。MYB转录因子FLP通过结合E2F关键靶基因的启动子区域抑制其转录，进而约束保卫母细胞的对称分裂。我们发现FLP有两种剪切形式，带有一个额外外显子(E11)的FLPL不能结合DNA，但能够与E2F蛋白相互作用，促进其降解。E11与小鼠p19ARF结构相似，提示动植物中对E2F的调节机制可能是保守的，但分子机制尚不清楚。本研究将以flp突变体为切入点，解析FLPL-E2F的相互作用，探究FLPS/L协同调控E2F依赖的细胞周期激活的调控和研究FLPL促进E2F降解的分子机制。对FLPL-E2F在细胞周期进程中的相互作用机制的创新性地理解，将为多细胞生物体的发育研究提供重要理论支撑。

The development of multicellular organisms requires perfect coordination between cell division and cell differentiation. How this coordination is achieved, and the mechanisms by which developmental regulators talk to central cell cycle components (e.g. E2F) are key questions in biology today. The Arabidopsis stoma is a pore, and is formed by a pair of guard cells (GCs) derived by a single symmetric division, from a guard mother cell (GMC). The MYB factor FOUR LIPS (FLP) restricts the GMC symmetrical division by binding to DNA regulatory sequences and repressing transcription of key E2F targets. FLP is alternatively spliced, and we recently discovered that the FLP isoform (FLPL) with an extra exon (E11) does not bind DNA, but physically interacts with E2F proteins, promoting their degradation. E11 bares structural similarities with murine p19ARF, suggesting a conserved mechanism for E2F protein regulation. However, thus far, the molecular mechanisms of FLPL in regulating the transcriptional activity of E2F are largely unknown. In this proposal, flp mutants will be used to characterize the FLPL-E2F interaction, to investigate how FLPS/L modulates E2F-dependent cell cycle activation synergistically, and to understand how FLPL promotes E2F degradation. This study will permit us to gain novel understanding of the MYB-E2F interplay in cell cycle progression, with important consequences to development of multi-cellular organisms.