Genetic strategies to reveal system properties of patterning processes

适当的植物模式对于优化生长性能、植物结构和生物量、植物再生特性和干细胞分配是重要的。最近一系列令人惊叹的结果将看似独立的图案化过程联系起来，包括胚轴形成、分生组织组织、侧面器官定位和维管图案化与植物激素生长素的极地运输有关。在前人对生长素反应因子(ARF)研究的基础上，我们为研究生长素介导的构图过程的系统特性建立了优化的遗传背景：(1)在发现生长素在茎分生组织和叶片中的作用机制的等价性之后，我们利用了叶系统更好的实验和数学可及性。在这里，我们将使用新的可视化和独特的局部干扰工具来探索自我调节生长素模式的系统属性。具体地说，MP/ARF5在多个突变背景中的空间和时间高度受控的活性可以作为一个理想的开关，在许多位置开启/关闭生长素介导的图案。因为在茎分生组织中具有相同的机制，所以这些发现将对整个茎分生组织结构产生影响。(2)在一系列相辅相成的研究中，我们确定了五个具有激活(富含Q的)中间结构域的ARF在构图过程中的相对贡献，包括直接靶基因和与AUX/IAA家族的共同调节因子相互作用的节点。(3)沿着第三条线，我们已经确定了ARF功能的第一个抑制因子，并对其进行了分子表征，该抑制因子定义了一条基本上未知的拮抗途径。我们将使用遗传和分子方法探索这一途径和其他ARF拮抗途径。最后，(4)我们对ARF调控下游早期血管发育基因的基因组工作引导我们探索血管组织规范中转录因子的层次结构。

Proper plant patterning is important for optimized growth performance, plant architecture and biomass, plant regeneration properties and stem cell allocation. An amazing suite of recent results has linked seemingly separate patterning processes, including embryo axis formation, meristem organization, lateral organ positioning and vascular patterning to the polar transport of the phyotohormone auxin. Based on previous work on Auxin Response Factors (ARFs) we have set up optimized genetic backgrounds for investigating the systems properties of auxin mediated patterning processes: (1) After discovering the equivalence of auxin foucssing mechanisms in the shoot meristem and in leaves, we are taking advantage of the better experimental and mathematical accessibility of the leaf system. Here we will explore the systems properties of self-regulatory auxin patterning, using novel visualization and unique local interference tools. Specifically, spatially and temporally highly controlled activity of MP/ARF5 in multiple mutant background can serve as an ideal switch to turn on/off auxin mediated patterning in numerous locations. Because equivalent mechanisms in the shoot meristem, the findings will have implications for the entire shoot architecture. (2) In a complementing line of research, we have identified the relative contributions of five ARFs with activating (Q-rich) middle domains in patterning processes, including immediate target genes and nodes of interaction with co-regulators of the Aux/IAA family. (3) Along a third line, we have identified and molecularly characterized a first suppressor of ARF function, which defines a largely unexplored antagonistic pathway. We will explore this and other ARF antagonizing pathways using genetic and molecular approaches. Finally, (4) our genomic work on genes in early vascular development downstream of ARF regulation leads us into the exploration of the transcription factor hierarchy in vascular tissue specification.