Niwa Tomoko, Kondo Tatsuhiko, Nishizawa Michi, Kajita Ryoko, Kakimoto Tatsuo, Ishiguro Sumie
Department of Biological Mechanisms and Functions, Graduate School of Bioagricultural Sciences, Nagoya University, Nagoya, Japan.
Biosci Biotechnol Biochem. 2013;77(6):1287-95. doi: 10.1271/bbb.130145. Epub 2013 Jun 7.
Stomatal development in Arabidopsis epidermis is both positively and negatively regulated by a family of Cys-rich peptides, EPIDERMAL PATTERNING FACTOR LIKEs (EPFLs). We synthesized biologically active synthetic EPFL5 (sEPFL5) peptide, which reduced the number of stoma in leaves and cotyledons. The sEPFL5 possesses three disulfide bonds at positions identical to those of a positive development factor, stomagen. Application of sEPFL5 had little inhibitory effect on protodermal cells entering the stomatal lineage, but did inhibit the maintenance of meristemoid activity, resulting in the differentiation of arrested meristemoids into pavement cells. This phenotype was enhanced in the too many mouths (tmm) mutant background. RNA analysis revealed that sEPFL5 application halved SPEECHLESS expression and abolished MUTE expression in tmm mutants, explaining the phenotype observed. The action of sEPFL5 was mediated by ERECTA family receptors. We propose that EPFL5 functions to establish the differentiation of stomatal lineage cells to pavement cells.
拟南芥表皮中的气孔发育受到一类富含半胱氨酸的肽——表皮模式因子类似物（EPFLs）的正向和负向调控。我们合成了具有生物活性的合成EPFL5（sEPFL5）肽，它减少了叶片和子叶中的气孔数量。sEPFL5在与正向发育因子气孔素相同的位置具有三个二硫键。sEPFL5的应用对进入气孔谱系的原表皮细胞几乎没有抑制作用，但确实抑制了分生组织细胞活性的维持，导致停滞的分生组织细胞分化为扁平细胞。在“太多嘴巴”（tmm）突变体背景下，这种表型增强。RNA分析表明，在tmm突变体中应用sEPFL5使SPEECHLESS表达减半并消除了MUTE表达，这解释了观察到的表型。sEPFL5的作用由ERECTA家族受体介导。我们提出EPFL5的功能是建立气孔谱系细胞向扁平细胞的分化。
