Hillmer, Rachel2018-07-262018-07-262016-04https://hdl.handle.net/11299/198389University of Minnesota Ph.D. dissertation. April 2016. Major: Plant Biological Sciences. Advisor: Fumiaki Katagiri. 1 computer file (PDF); x, 140 pages.Systems biology is the study of how biological systems operate as a whole. Systems become complex when interactions between system parts dominate system behavior. To uncover the mechanisms by which complex biological systems operate, those interactions must be discovered and quantified. Further, to understand dynamic system behavior, mechanistic rules for how system parts are stimulated and regulate each other must be discovered. The plant immune signaling network, which protects plants from pathogens, is an especially complex system. Pathogens disable plant immune signaling with effectors; thus plant immunity must be robust against pathogen perturbation. Thus, deciphering the mechanisms that underlie the plant immune signaling network is met by a challenge: effects of single-gene mutations, on which traditional genetic analysis depends, are also buffered by the network. In this dissertation, a network reconstitution approach was taken, where the network is disassembled and then stepwise re-assembled, to accurately assign network functions to system parts, including interactions between parts. We define the plant immune signaling network in terms of 4 major signaling sectors controlled by the plant hormones jasmonate (JA), ethylene (ET), and salicylate (SA) sectors, and the major immune regulator phytoalexin-deficient 4 (PAD4). Dynamic transcriptome and hormone profiles after plant immune stimulus with bacterial flagellin were collected across a combinatorially complete set of mutants, lacking all combinations of these four sectors. These mutant profiles were used in (1) attempts to find mechanistic mathematical models of immune network behavior and to (2) characterize the four-sector network’s control of the flg22-responsive transcriptome. The work in this dissertation produced two main discoveries. First, that delay differential equations (DDEs) can be found which provide mechanistic explanations of immune network function; additional time course detail will be needed to confirm the accuracy of these models. Second, network buffering is extensive in the flg22-responsive transcriptome. As a result of this network buffering, our network reconstitution based interpretations of gene regulation are at points quite different from the regulatory mechanisms described in the plant immunity literature.enmathematical modelingnetwork bufferingplant immune signaling networksystems biologyThesis or Dissertation