The establishment of the cambium-specific stem cell niche, which is being addressed by characterizing CBI1, a novel repressor of cambium identity in Arabidopsis thaliana

维管形成层是植物生物量生产的重要组织，在植物生长和当前植物研究中具有重要意义，是研究分生组织调控的独特系统。有趣的是，尽管植物激素生长素与促进形成层的形成和活性之间已经建立了良好的联系，但直到最近才通过转录因子WOX4描述了形成层本身水平上的分子联系（Suer et al., 2011）。在这个项目中，我们将利用CAMBIUM ISLANDS1 (CBI1)，一个参与WOX4调控的新位点来解决细胞如何在WOX4上游建立分生组织活性的问题。我们在WOX4:GUS报告基因活性改变的突变体的正向遗传学筛选中发现了cbi1突变体。cbi1突变体以两个隐性等位基因为代表，在茎髓组织中表现出岛状异位WOX4:GUS活性，与细胞模式缺陷重叠。此外，cbi1茎显示出（亲）形成层特异性基因ATHB8、PXY和WOX4以及生长素诱导基因PIN1和IAA5的转录水平增强，这表明cbi1在抑制整个形成层身份过程中发挥了普遍作用。基于这些观察，我假设CBI1在生长素生物合成、运输或信号传导的上游发挥作用。由于迄今为止还没有描述过这样一种通用的血管调节剂，因此揭示CBI1在已知形成层调节剂网络中的功能将是非常重要的。通过在组织学和分子水平上详细的突变分析，CBI1位点的鉴定，随后的表达研究，以及通过揭示CBI1与生长素生物合成、运输和信号传导的联系，该项目有可能为血管模式和细胞规范的早期事件提供长期寻求的见解。

The vascular cambium, being an essential tissue for plant biomass production, is of extraordinary importance for plant growth and current plant research, and represents a unique system to study meristem regulation. Interestingly, despite the well-established connection between the plant hormone auxin and the promotion of cambium initiation and activity, a molecular link on the level of the cambium itself has only recently been described by the transcription factor WOX4 (Suer et al., 2011). In this project, we will make use of CAMBIUM ISLANDS1 (CBI1), a novel locus involved in WOX4 regulation to address the question of how cells establish meristematic activity, upstream of WOX4. We identified cbi1 mutants in a forward genetics screen for mutants with altered activity of a WOX4:GUS reporter. Represented by two recessive alleles, cbi1 mutants display island-like ectopic WOX4:GUS activity in the pith tissue of stems, overlapping with cellular patterning defects. Furthermore, cbi1 stems show enhanced transcript levels of the (pro)cambium-specific genes ATHB8, PXY, and WOX4, and the auxin-inducible genes PIN1 and IAA5, suggesting a general role of CBI1 in repressing the entire program of cambium identity. Based on these observations, I hypothesize that CBI1 functions upstream of auxin biosynthesis, transport, or signaling. Because such a general vascular regulator has so far not been described, revealing the function of CBI1 within the network of known cambium regulators will be highly significant. By detailed mutant analysis on both histological and molecular levels, identification of the CBI1 locus, subsequent expression studies, and by unraveling the connection of CBI1 with auxin biosynthesis, transport, and signaling, the project has the potential to deliver long-sought insights into the early events of vascular patterning and cell specification.