Plant vascular cell division is maintained by an interaction between PXY and ethylene signalling.
Plant vascular cell division is maintained by an interaction between PXY and ethylene signalling.
复制标题
通过PXY和乙烯信号传导之间的相互作用来维持植物血管细胞分裂。
DOI：
10.1371/journal.pgen.1002997
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发表时间：
2012
期刊：
影响因子：
4.5
通讯作者：
Turner SR
中科院分区：
文献类型：
--
作者：
Etchells JP;Provost CM;Turner SR
原形成层和形成层是维管组织起源的分生组织。维管原始细胞在茎的外侧分化为韧皮部，在茎的内侧分化为木质部。来自CLV-3/ESR 1-LIKE 41（CLE 41）的小肽被认为通过木质部间质（PXY）受体激酶的信号传导促进维管分生组织中的细胞分裂。然而，pxy突变体仅显示出维管细胞数量的少量减少，这表明存在允许植物补偿PXY缺失的机制。与这一想法相一致，我们确定了大量的基因特异性上调pxy突变体，包括几个AP 2/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上调乙烯和乙烯过量生产eto 1突变体。eto 1突变体还表现出依赖于这些ERF基因中至少2个的功能的血管细胞分裂的增加。此外，使用各种乙烯不敏感突变体如ein 2阻断乙烯信号传导增强了pxy的细胞分裂缺陷。我们的研究结果表明，这些因素定义了一个新的途径，平行于PXY/CLE 41调节发育中的血管组织的细胞分裂。我们提出了一个模型，即血管细胞分裂的PXY信号和乙烯/ERF信号调节。然而，在正常情况下，PXY信号传导起到抑制乙烯/ERF途径的作用。植物通过一个专门的血管系统在体内运输水分和营养物质。维管组织还负责为植物提供结构支持;例如，木材由专门的维管细胞组成。因此，维管系统构成了植物生物量的大部分。从植物生物质中提取的化学品可用于制造下一代生物燃料，以减少对化石燃料的依赖。维管组织来源于一组存在于称为原形成层的结构中的分裂细胞，但对该结构中控制细胞分裂的机制仍知之甚少。了解原形成层中发生的事件可能有助于我们了解如何最好地利用植物来增加植物生物量，例如用于生物燃料和木材生产。我们已经确定了一些基因，调节细胞分裂的原形成层是由气态植物激素乙烯控制。我们表明，乙烯信号，反过来，与PXY，一个基因编码的信号成分，也控制血管细胞分裂相互作用。我们的研究结果表明，乙烯和PXY信号之间的相互作用是负责维持植物维管系统。
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. Plants transport water and nutrients throughout their bodies using a specialised vascular system. Vascular tissue is also responsible for providing structural support to plants; for example, wood is made up of specialised vascular cells. Consequently, the vascular system constitutes the majority of plant biomass. Chemicals from plant biomass could be used to make the next generation of biofuels in order to reduce dependence on fossil fuels. Vascular tissue is derived from a group of dividing cells present in a structure called the procambium, but mechanisms controlling cell division in this structure remain poorly understood. Understanding the events that occur in the procambium may help us to understand how we can best utilise plants for increased plant biomass, for example, for biofuel and wood production. We have identified a number of genes that regulate cell division in the procambium that are controlled by the gaseous plant hormone ethylene. We show that ethylene signalling, in turn, interacts with PXY, a gene encoding a signalling component that also controls vascular cell division. Our results demonstrate that the interaction between ethylene and PXY signalling is responsible for maintaining the plant vascular system.
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