Regulation of planar growth during integument development of Arabidopsis thaliana.

• Applicant: Professor Dr. Kay Schneitz
• Subject Area: Plant Cell and Developmental Biology
• Term: from 2013 to 2018
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 241884464

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.

• DFG Programme: Research Grants