Regulation of planar growth during integument development of Arabidopsis thaliana.

平面生长是组织层内细胞分裂模式的协调，对植物组织形态发生至关重要。单个组织层，如表皮，由不对称或形成性分裂启动。相反，对称分割，即分裂产生两个具有相同身份的子细胞，保持层。人们对沿着表皮平面定向对称分割面的发育控制知之甚少。拟南芥胚珠被是研究这一过程的一个很好的模型系统。我们以前的工作表明，拟南芥AGC蛋白激酶独角兽(UCN)抑制了珠被和其他花组织中局部的异位生长，并保持了平面生长。我们的数据表明，UCN通过直接抑制Kanadi转录因子异常Testa Shape(ATS)来控制这些过程。ATS参与控制珠被的突起和近、远轴方向的极性。在Ucn突变体中未能抑制ATS被预测会导致ATS的过度活跃和转录程序的错误调控，这反过来又会导致异常的分裂平面和异位突起的形成。现在的中心目标是了解在珠被发育过程中UCN介导的平面生长控制的分子细节。为此，我们已经使用两种不偏不倚的方法确定了UCN信令网络的其他候选组件。在酵母双杂交系统的帮助下，我们确定了UCN的两个可能的相互作用因子：AGC蛋白激酶PDK1和肌球蛋白SNAG。有趣的是，PDK1的突变抑制了UCN表型，而SNAG-1突变体的胚珠与UCN突变体的胚珠相似。这些结果为PDK1和SNAG参与UCN机制提供了额外的证据。此外，我们在遗传UCN抑制子筛选中确定了三个基因座。在这个项目中，我们将结合遗传学、分子生物学、生化和细胞生物学的方法，对UCN介导的信号转导有一个更全面的了解。第一个目标是进一步研究UCN的功能，更深入地探讨UCN和ATS之间的相互作用。第二个目标是证实UCN、PDK1和SNAG之间的相互作用，并评估潜在的分子机制。第三个目标是识别和表征三个UCN抑制基因座，并研究它们与UCN信令网络中其他已知成员的关系。

Planar growth, the coordination of cell division patterns within a tissue layer, is essential to plant tissue morphogenesis. A single tissue layer, such as the epidermis, is initiated by asymmetric or formative divisions. By contrast, symmetric divisions, where division results in two daughter cells of equal identity, maintain the layer. Little is known about the developmental controls that orient symmetric division planes along the plane of the epidermis. Integuments of Arabidopsis ovules represent an excellent model system to study this process. Our previous work revealed that the Arabidopsis AGC protein kinase UNICORN (UCN) suppresses localized ectopic outgrowth and maintains planar growth in integuments and other floral tissues. Our data suggest that UCN controls these processes by directly inhibiting the KANADI transcription factor ABERRANT TESTA SHAPE (ATS). ATS is involved in the control of the outgrowth and adaxial-abaxial polarity of integuments. Failure to repress ATS in ucn mutants is predicted to result in hyperactive ATS and misregulation of transcriptional programs, which in turn results in aberrant division planes and ectopic outgrowth formation. The central objective now is to understand the molecular details of UCN-mediated control of planar growth during integument development. To this end we have already identified additional candidate components of the UCN signaling network using two unbiased approaches. With the help of a yeast two-hybrid system we identified two putative interactors of UCN: the AGC protein kinase PDK1 and the myosin SNAG. Interestingly, mutations in PDK1 suppress the ucn phenotype while ovules of a snag-1 mutant resemble ovules from ucn mutants. These results provide additional evidence for an involvement of PDK1 and SNAG in the UCN mechanism. In addition, we genetically identified three loci in a genetic ucn suppressor screen. In this project, using a combination of genetic, molecular, biochemical and cell biological approaches, we will gain a more comprehensive knowledge about UCN-mediated signaling. The first goal is to investigate further UCN function and to probe deeper into the interaction between UCN and ATS. A second goal is to corroborate the interaction between UCN, PDK1 and SNAG and assess the underlying molecular mechanisms. The third goal is to identify and characterize the three ucn suppressor loci and to study their relationship with the other known members of the UCN signaling network.