Epidermal Cell Density is Autoregulated via a Secretory Peptide, EPIDERMAL PATTERNING FACTOR 2 in Arabidopsis Leaves

Epidermal Cell Density is Autoregulated via a Secretory Peptide, EPIDERMAL PATTERNING FACTOR 2 in Arabidopsis Leaves
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DOI:
10.1093/pcp/pcp068
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发表时间:
2009-06-01
影响因子:
4.9
通讯作者:
Kakimoto, Tatsuo
Kakimoto, Tatsuo
中科院分区:
生物学2区
文献类型:
--
作者:
Hara, Kenta;Yokoo, Toshiya;Kakimoto, Tatsuo

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细胞数量的调节对于多细胞生物的发育至关重要。在植物表皮发育过程中,原真皮细胞首先做出是否成为分生组织母细胞(MMC)的命运决定,MMC经历不对称细胞分裂形成分生组织及其姐妹细胞。 MMC 衍生谱系产生所有气孔保卫细胞和大部分非保卫细胞。我们证明了一种小分泌肽,表皮图案因子 2 (EPF2),由 MMC 及其早期后代产生,并对保卫和非保卫表皮细胞的密度产生负调节。我们的结果表明,EPF2 以非细胞自主方式抑制细胞采用 MMC 命运,从而限制 MMC 的数量。该反馈回路对于表皮细胞密度的调节至关重要。 EPF2 的氨基酸序列与 EPF1 相似,已知 EPF1 可以控制气孔定位。 EPF1的过度表达也会抑制气孔发育,但EPF1只能作用于比EPF2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,而不是基因的表达模式,决定了特定的功能。尽管 EPF1 和 EPF2 的靶点不同,但 EPF1 和 EPF2 都需要共同的假定受体成分 TOO MANY MOUTHS (TMM)、ERECTA (ER)、ERECTA LIKE 1 (ERL1) 和 ERL2 才能发挥作用。
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.