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，是植物组织形态建成的必要条件。一个单一的组织层，如表皮，是由不对称的或形成的分裂开始的。相比之下，对称分裂，分裂产生两个相同的子细胞，保持层。很少有人知道的发展控制定向对称分裂平面沿着平面的表皮。拟南芥胚珠被是研究这一过程的理想模型。我们以前的工作表明，拟南芥AGC蛋白激酶UNICORN（UCN）抑制局部异位生长，维持珠被和其他花组织的平面生长。我们的数据表明，UCN通过直接抑制KANADI转录因子ABERRANT TESTA SHAPE（ATS）来控制这些过程。ATS参与珠被的生长和近轴-远轴极性的控制。预测在ucn突变体中未能抑制ATS会导致ATS过度活跃和转录程序的失调，这反过来又会导致异常的分裂平面和异位生长形成。现在的中心目标是了解珠被发育过程中UCN介导的平面生长控制的分子细节。为此，我们已经确定了UCN信令网络的其他候选组件使用两个无偏的方法。借助酵母双杂交系统，我们确定了UCN的两个假定相互作用因子：AGC蛋白激酶PDK 1和肌球蛋白SNAG。有趣的是，PDK 1突变抑制ucn表型，而snag-1突变体的胚珠类似于ucn突变体的胚珠。这些结果为PDK 1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、生物化学和细胞生物学的方法，对UCN介导的信号传导有更全面的了解。第一个目标是进一步研究UCN的功能，并深入探讨UCN和ATS之间的相互作用。第二个目标是证实UCN，PDK 1和SNAG之间的相互作用，并评估潜在的分子机制。第三个目标是确定和表征三个ucn抑制基因座，并研究它们与UCN信号网络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.