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Abstract

It is the aim of this thesis to analyze the initiation and regulation of the fast brassinosteroid response pathway Arabidopsis thaliana and its role for cell elongation in an integrative fashion using mathematical modeling. Brassinosteroids are plant steroid hormones that mediate various physiological and developmental processes. One of these processes is cell elongation, which is the major mechanism for organ growth in plants. As sessile organisms, plants have to rely on growth to open up new resources. However, growth is an energy consuming process that has to be tightly regulated. Therefore, it is necessary to understand the activation and regulation of the fast brassinosteroid response. The computational modeling and analysis of the fast brassinosteroid signaling focused on several different aspects. Because of the importance of compartmentalization in biological systems, I first studied the different modeling approaches to describe multi-compartment processes in models consisting of ordinary differential equations and how these modeling approaches react to changes in cell morphology. This analysis shows that including the membrane as interaction area can be crucial to proper modeling behavior depending on the modeled system. Second,I used molecular modeling to clarify the interactions between receptor, co-receptor and a negative regulator of the fast brassinosteroid response. Here, the simulated complexes show that the negative regulator acts by blocking the catalytic domain of the co-receptor, which is then unable to participate in propagating the signal. Third, I used a dynamic model consisting of ordinary differential equations to simulate the fast brassinosteroid response on a cellular scale. The parameters of this model were fitted to dose-response data of the membrane potential change. Furthermore, this model includes the BR-induced increase in cell wall volume. I validated this model with respect to the behavior in the meristematic root zone and the behavior in a deletion of a negative regulator. Based on the model behavior and the quantification of model species, we hypothesize that H+-ATPase levels in the different root zones determine the response to brassinosteroid stimulation in the fast response pathway. Finally, I expanded the ordinary differential equation model for the fast brassinosteroid response to include the process of cell elongation. This model can describe the experi- mentally observed elongation behavior of an epidermis cell from the meristematic zone to the final cell length in the maturation zone. I combined this model with an agent-based representation of the root. This model provides an integrative view on cell elongation. While this multi-scale model is currently limited to one cell type and a maximal cell length of 25µm, this shows that it is a valid approach to modeling root elongation.