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。最近一系列令人惊讶的结果将看似独立的模式化过程联系起来，包括胚轴形成，分生组织，侧向器官定位和维管模式与植物激素生长素的极性运输。在前人对生长素反应因子（ARF）研究的基础上，我们建立了优化的遗传背景，用于研究生长素介导的模式化过程的系统特性：（1）在发现生长素在茎分生组织和叶片中聚集机制的等价性后，我们利用了叶片系统更好的实验和数学可及性。在这里，我们将探索自我调节生长素图案的系统特性，使用新的可视化和独特的本地干扰工具。具体地说，MP/ARF 5在多个突变体背景中的空间和时间上高度受控的活性可以作为理想的开关来打开/关闭生长素介导的许多位置的图案化。由于茎分生组织中存在类似的机制，这些发现将对整个茎结构产生影响。 (2)在一个补充线的研究，我们已经确定了五个ARF的激活（Q-丰富）的中间域的图案化过程中，包括直接靶基因和节点的相互作用与辅助/IAA家族的共调节的相对贡献。(3)沿着第三条线，我们已经确定和分子特征的第一个抑制剂的ARF功能，它定义了一个很大程度上未开发的拮抗途径。我们将利用遗传学和分子生物学的方法来探索这种和其他ARF拮抗途径。最后，（4）我们对ARF调控下游的早期血管发育基因的基因组学研究使我们进入了血管组织特化中转录因子层次的探索。

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.