Hara Kenta, Yokoo Toshiya, Kajita Ryoko, Onishi Takaaki, Yahata Saiko, Peterson Kylee M, Torii Keiko U, Kakimoto Tatsuo
Department of Biological Science, Graduate School of Sciences, Osaka University, Toyonaka, Osaka, Japan.
Plant Cell Physiol. 2009 Jun;50(6):1019-31. doi: 10.1093/pcp/pcp068. Epub 2009 May 12.
Regulation of the number of cells is critical for development of multicellular organisms. During plant epidermal development, a protodermal cell first makes a fate decision of whether or not to be the meristemoid mother cell (MMC), which undergoes asymmetric cell division forming a meristemoid and its sister cell. The MMC-derived lineage produces all stomatal guard cells and a large proportion of non-guard cells. We demonstrate that a small secretory peptide, EPIDERMAL PATTERING FACTOR 2 (EPF2), is produced by the MMC and its early descendants, and negatively regulates the density of guard and non-guard epidermal cells. Our results suggest that EPF2 inhibits cells from adopting the MMC fate in a non-cell-autonomous manner, thus limiting the number of MMCs. This feedback loop is critical for regulation of epidermal cell density. The amino acid sequence of EPF2 resembles that of EPF1, which is known to control stomatal positioning. Over-expression of EPF1 also inhibits stomatal development, but EPF1 can act only on a later developmental process than EPF2. Overexpression and promoter swapping experiments suggested that the protein functions of EPF1 and EPF2, rather than the expression patterns of the genes, are responsible for the specific functions. Although targets of EPF1 and EPF2 are different, both EPF1 and EPF2 require common putative receptor components TOO MANY MOUTHS (TMM), ERECTA (ER), ERECTA LIKE 1 (ERL1) and ERL2 in order to function.
细胞数量的调控对于多细胞生物的发育至关重要。在植物表皮发育过程中,一个原表皮细胞首先要做出是否成为分生组织母细胞(MMC)的命运决定,MMC会进行不对称细胞分裂,形成一个分生组织细胞及其姐妹细胞。MMC衍生的细胞谱系产生所有的气孔保卫细胞和大部分非保卫细胞。我们证明,一种小分泌肽表皮模式因子2(EPF2)由MMC及其早期后代产生,并负向调节保卫细胞和非保卫表皮细胞的密度。我们的结果表明,EPF2以非细胞自主的方式抑制细胞采用MMC命运,从而限制MMC的数量。这种反馈回路对于调节表皮细胞密度至关重要。EPF2的氨基酸序列与已知控制气孔定位的EPF1相似。EPF1的过表达也会抑制气孔发育,但EPF1只能作用于比EPF2更晚的发育过程。过表达和启动子交换实验表明,EPF1和EPF2的蛋白质功能而非基因的表达模式决定了它们的特定功能。虽然EPF1和EPF2的作用靶点不同,但EPF1和EPF2发挥功能都需要共同的假定受体组分过多的口(TMM)、直立(ER)、类直立1(ERL1)和ERL2。