WUSCHEL: the versatile protein in the shoot apical meristem
WUSCHEL: the versatile protein in the shoot apical meristem
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WUSCHEL：茎尖分生组织中的多功能蛋白质
DOI：
10.1007/s11427-020-1870-4
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发表时间：
2020-12
期刊：
影响因子：
--
通讯作者：
Xu Lin
中科院分区：
文献类型：
--
作者：
Xu Lin
在维管植物中，几乎所有的地上器官都来源于茎顶端分生组织（SAM）。SAM的发育作用已被广泛研究，特别是在模式双子叶植物拟南芥中（Aichinger et al.，2012年）。SAM在空间上分为三个区域：中心区，包括干细胞和组织中心（OC）;外围区，可以启动侧附属物，如叶和花;和肋区，位于中心区和外围区下方。在中央区域，OC向干细胞提供信号并维持其活性。反过来，干细胞提供信号来限制OC中细胞的数量。此外，SAM含有肋分生组织活性，这是负责节间的形成。引人注目的是，SAM也是一个无病毒区域。已知病毒颗粒的积累朝向SAM减少，并且这导致了通过SAM组织培养来培养无病毒植物的技术的发展（Morel和Martin，1952）。然而，目前还不清楚为什么以及如何SAM保持无病毒。最近，由Zhao和Tian领导的研究小组通过表征WUSCHEL（WUS）转录因子在确定SAM无病毒性质的分子机制方面取得了很大进展（Wu et al.，2020年）。WUS是在WUSCHELRELATED HOMEOBOX（WOX）转录因子家族中鉴定的第一个基因（Mayer等人，1998年）。WUS中的突变导致更小和更不活跃的SAM。WUS基因在OC中表达，并且WUS蛋白可以从OC移动到外部区域，例如OC上方的干细胞（Yadav等人，2011年）。在干细胞中，WUS与SHOOT MERISTEMLESS（STM）相互作用并促进CLAVATA 3（CLV 3）的表达以控制干细胞活性（Su et al.，2020年）。进而，CLV 3通过其信号传导途径将WUS表达限制于OC，从而在干细胞和OC之间形成反馈环（弗莱彻等人，1999; Schoof等人，2000）。因此，WUS转录因子似乎是SAM发育过程中中央区细胞身份的关键调节因子。最近，Wu等人（2020）通过将WUS与病毒控制联系起来，在理解SAM的抗病毒机制方面迈出了重要一步。他们观察到黄瓜花叶病毒（CMV）可以感染拟南芥的许多组织，但不能感染SAM或花分生组织（FM）。在clv 3突变体中，WUS在L2细胞层异位表达，CMV可以向上移动到含有WUS的组织下方的区域。当CMV被引入到表现出大SAM的mp clv 3双突变体的干细胞和OC区域中时，CMV颗粒仍然能够扩散到干细胞和OC区域下方的区域中，但不会在含有WUS的组织中积累。异位积累的WUS可抑制CMV在干细胞和OC外的表达，下调WUS表达可导致CMV在整个SAM内的积累。WUS蛋白也可由CMV感染在涉及外周带和FM的更广泛区域中诱导。因此，作者认为WUS可能在抑制病毒积累方面发挥作用，但不是病毒传播。
In vascular plants, almost all above-ground organs are derived from the shoot apical meristem (SAM). The developmental role of the SAM has been extensively studied, especially in the model dicot plant Arabidopsis thaliana (Aichinger et al., 2012). The SAM is spatially divided into three regions: the central zone comprising the stem cells and the organizing center (OC); the peripheral zone that can initiate lateral appendages such as leaves and flowers; and the rib zone that is located beneath the central zone and the peripheral zone. In the central zone, the OC provides signals to the stem cells and maintains their activity. In turn, the stem cells provide signals to restrict the number of cells in the OC. In addition, the SAM contains rib meristem activity, which is responsible for internode formation. Strikingly, the SAM is also a virus-free region. It is known that the accumulation of virus particles decreases toward the SAM, and this has led to the development of technologies to culture virus-free plants by SAM tissue culture (Morel and Martin, 1952). However, it is unclear why and how the SAM remains free of viruses. Recently, research groups led by Zhao and Tian have made great progress in determining the molecular mechanism of the virus-free nature of the SAM by characterizing the WUSCHEL (WUS) transcription factor (Wu et al., 2020). WUS was the first gene to be identified in the WUSCHELRELATED HOMEOBOX (WOX) transcription factor family (Mayer et al., 1998). Mutations inWUS lead to a smaller and less active SAM. TheWUS gene is expressed in the OC, and the WUS protein can move from the OC to outer regions such as the stem cells above the OC (Yadav et al., 2011). In the stem cells, WUS interacts with SHOOT MERISTEMLESS (STM) and promotes the expression of CLAVATA3 (CLV3) to control stem cell activity (Su et al., 2020). In turn, CLV3 confines WUS expression to the OC through its signaling pathway, thus forming a feedback loop between stem cells and the OC (Fletcher et al., 1999; Schoof et al., 2000). Therefore, the WUS transcription factor appears to be a key regulator of cell identity in the central zone during SAM development. Recently, Wu et al. (2020) made a great step toward understanding the anti-virus mechanism of the SAM by linking WUS to virus control. They observed that cucumber mosaic virus (CMV) could infect many tissues in Arabidopsis, but not the SAM or the floral meristem (FM). In the clv3mutant, in whichWUS was ectopically expressed in the L2 cell layer, CMV could move upwards to the region beneath the tissues containing WUS. When CMV was introduced into the stem cells and the OC region of the mp clv3 double mutant, which exhibited a large SAM, CMV particles were still able to spread into the region beneath the stem cells and the OC region, but did not accumulate in WUS-containing tissues. Ectopically accumulated WUS could inhibit CMVoutside of the stem cells and the OC, and down-regulation of WUS resulted in the accumulation of CMV throughout the whole SAM. The WUS protein could also be induced by CMV infection in a broader region involving the peripheral zone and the FM. Therefore, the authors suggested that WUS may have a role in inhibiting virus accumulation, but not virus spread.
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DOI：
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发表时间：
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期刊：
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影响因子：
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期刊：
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发表时间：
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期刊：
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