Polycomb repressive complex 2 (PRC2)介导的基因沉默表达对生物生长发育非常重要。模式植物拟南芥中PRC2的功能缺失导致转型失控和发育异常。PRC2本身无识别DNA能力，因此PRC2如何被招募到靶基因上的分子机理仍然不十分清楚。我们前期鉴定到与PRC2催化亚基SWN互作的2个转录因子SITF1和SITF2，发现sitf1 sitf2的表型和转录组与PRC2催化亚基的双突变体swn clf相似，且sitf1 sitf2中H3K27me3的分布发生显著变化。因此我们推测SITF1/2可能招募PRC2对靶基因进行Polycomb沉默。本项目拟系统研究STIF1/2在介导Polycomb沉默靶基因中所起的作用，阐明它们是否以及招募PRC2到靶基因的分子机制。本项目的完成将发现植物PRC2识别靶基因的新机制，对理解PRC2复合体调节植物基因表达的机理具有重要理论意义。

Polycomb repressive complex 2 (PRC2) mediated gene silencing plays a critical role in the growth and development of eukaryotes. Mutation of Arabidopsis PRC2 leads to failed transition and severe abnormal morphological phenotypes. Given that PRC2 has no inherent DNA binding specificity, the underlying molecular mechanism by which PRC2 targets the loci it silences still remains obscure. We previously identified two transcription factors SITF1 and SITF2 that interact with the PRC2 catalytic subunit SWN, and found that sitf1 sitf2 double mutants display phenotypes and transcriptome pattern that are closest to those of the PRC2 catalytic subunit double mutants swn clf. Moreover, the genome-wide H3K27me3 distribution in sitf1 sitf2 changes significantly. Hence, we hypothesized that SITF1/2 could recruit SWN-PRC2 for mediating Polycomb silencing at target loci. In this proposal, we aim to investigate the role of SITF1/2 in mediating PRC2 silencing and decipher the molecular mechanism by which SITF1/2 recruits PRC2 to silence target gene. This work will discover novel mechanisms by which plant PRC2 recognizes its loci, and greatly enhance our understanding on the role of PRC2 in regulating gene expression in plants.