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，在植物生长和现代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形成层起始和活性的促进之间的良好建立的联系，但形成层本身水平上的分子连接最近才被转录因子WOX 4描述（Suer等人，2011年）。在这个项目中，我们将利用CAMBIUM ISLANDS1（CBI1），一个新的基因座参与WOX4的调控，以解决细胞如何建立分生组织活性的问题，上游的WOX4。我们确定了cbi1突变体的正向遗传学筛选的突变体与改变活性的WOX4：GUS报告。由两个隐性等位基因，cbi1突变体显示岛状异位WOX4：GUS活性在茎髓组织，重叠与细胞图案缺陷。此外，cbi 1茎显示增强的（原）形成层特异性基因ATHB 8，PXY和WOX 4，以及生长素诱导基因PIN 1和IAA5的转录水平，这表明CBI 1在抑制形成层身份的整个程序中的一般作用。基于这些观察，我假设CBI1的功能上游生长素的生物合成，运输，或信号。由于这样一个通用的血管调节器迄今尚未被描述，揭示CBI1在已知的形成层调节器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进行详细的突变分析，CBI1基因座的鉴定，随后的表达研究，以及通过解开CBI1与生长素生物合成，运输和信号传导的联系，该项目有可能提供长期寻求的对血管图案和细胞特化的早期事件的见解。

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.