Faculty of Life Sciences, University of Manchester, Manchester, United Kingdom.
PLoS Genet. 2012;8(11):e1002997. doi: 10.1371/journal.pgen.1002997. Epub 2012 Nov 15.
The procambium and cambium are meristematic tissues from which vascular tissue is derived. Vascular initials differentiate into phloem towards the outside of the stem and xylem towards the inside. A small peptide derived from CLV-3/ESR1-LIKE 41 (CLE41) is thought to promote cell divisions in vascular meristems by signalling through the PHLOEM INTERCALLATED WITH XYLEM (PXY) receptor kinase. pxy mutants, however, display only small reductions in vascular cell number, suggesting a mechanism exists that allows plants to compensate for the absence of PXY. Consistent with this idea, we identify a large number of genes specifically upregulated in pxy mutants, including several AP2/ERF transcription factors. These transcription factors are required for normal cell division in the cambium and procambium. These same transcription factors are also upregulated by ethylene and in ethylene-overproducing eto1 mutants. eto1 mutants also exhibit an increase in vascular cell division that is dependent upon the function of at least 2 of these ERF genes. Furthermore, blocking ethylene signalling using a variety of ethylene insensitive mutants such as ein2 enhances the cell division defect of pxy. Our results suggest that these factors define a novel pathway that acts in parallel to PXY/CLE41 to regulate cell division in developing vascular tissue. We propose a model whereby vascular cell division is regulated both by PXY signalling and ethylene/ERF signalling. Under normal circumstances, however, PXY signalling acts to repress the ethylene/ERF pathway.
原形成层和形成层是衍生维管组织的分生组织。维管原基向茎的外侧分化为韧皮部，向内侧分化为木质部。一种源自 CLV-3/ESR1-LIKE 41（CLE41）的小肽被认为通过与 PHLOEM INTERCALLATED WITH XYLEM（PXY）受体激酶的信号传导来促进维管分生组织的细胞分裂。然而，pxy 突变体仅显示维管束细胞数量的微小减少，这表明存在一种机制允许植物补偿 PXY 的缺失。与这一观点一致，我们鉴定了大量在 pxy 突变体中特异性上调的基因，包括几个 AP2/ERF 转录因子。这些转录因子是形成层和原形成层中正常细胞分裂所必需的。这些相同的转录因子也被乙烯和乙烯过表达的 eto1 突变体上调。eto1 突变体也表现出依赖于至少 2 个这些 ERF 基因功能的维管束细胞分裂增加。此外，使用各种乙烯不敏感突变体（如 ein2）阻断乙烯信号会增强 pxy 的细胞分裂缺陷。我们的结果表明，这些因子定义了一个新的途径，与 PXY/CLE41 平行作用于调节发育中的维管束组织的细胞分裂。我们提出了一个模型，即维管束细胞分裂既受 PXY 信号的调节，也受乙烯/ERF 信号的调节。然而，在正常情况下，PXY 信号起抑制乙烯/ERF 途径的作用。
