Environmental Regulation of Plant Stomatal Development By Cell Fate Morphogens in Arabidopsis thaliana

The rapid rise in atmospheric carbon dioxide (CO₂) levels suppresses the development of stomatal gas exchange pores in the aerial epidermis of plants. Scarce fresh water reserves for agriculture, rising temperatures and the elevated CO₂-repression of stomatal development amplify heat stress and can significantly affect plant carbon assimilation on a global scale. The underlying molecular mechanisms responsible for sensing atmospheric [CO₂] have remained unknown. Our new research on Arabidopsis thaliana carbonic anhydrase mutants, combined with biochemical and genetic experiments and candidate screening employing systems-level CO₂-dependent RNA-Seq, qPCR and cell wall proteomics have identified key components of this long-sought pathway. A framework of mechanisms was identified in which catalytic activity of carbonic anhydrases, the secreted peptide hormone EPF2 and its newly identified processing protease CRSP, act in concert to repress stomatal development at elevated CO₂. The CRSP protease functions as a key mediator of stomatal cell fate by cleaving and activating the EPF2 epidermal morphogen. We are employing systems biology approaches, combined with genetic perturbations of newly discovered candidate genes and mathematical modelling to generate a wealth of transcriptomic and proteomic datasets. Using novel algorithmic tools and these transcriptomic and proteomic “big” data, we aim to dissect the regulatory networks underlying CO₂ stress adaptation in plants and delve deeper into this CO₂ stress signaling pathway. New results from omics-level experiments and computational approaches will be presented along with data on the newly identified CO₂ signaling framework.