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Dynamic evolution in the Leucine-Rich Repeat Receptor-Like Kinase (LRR-RLK) family of receptors

Cells in multicellular organisms must gauge their environmental conditions, including neighboring cells, during development. In plants, the Leucine-Rich Repeat Receptor-like Kinases (LRR-RLKs) encode a family of membrane-bound receptors that transduce such cell-to-cell signals and are required for many aspects of plant development. Very little is known about the function of most of these genes, and the evolutionary history of the family is difficult to infer because of its size and complexity. Several factors contribute to this difficulty, including genetic redundancy, challenging bioinformatic detection, exceptionally large family size, and high copy number variation among species. In this dissertation, I characterize some of the evolutionary dynamics of this gene family, and contribute some methods for learning about their function and evolution. Chapter 1 is a brief introduction on LRR-RLKs, their evolution, and what obstacles hinder progress. In chapter 2, to address the incongruous gene trees found in published literature, I developed an improved approach to detect additional members of the gene family. This effort revealed many LRR-RLK structural variants absent from published trees, some of which were misclassified into other families. The technique developed for this project is applicable to any large and complex gene family in any organism, and highlights diverse evolutionary features of deep-time evolution. In chapter 3, I pose new questions about the domain-specificity of LRR-RLK evolution. I developed several techniques to discriminate different evolutionary trajectories of the protein domains themselves, including differential tests for selection, sequence evolutionary rates, and functional conservation. This revealed a pervasive difference between the LRR vs. RLK domains, favoring faster and adaptive evolution in LRR domains, which detect signals, and slower, functionally conserved evolution in RLK domains, which control cellular responses to signals. Taken together, these results support a model in which plants expand their developmental programs by gene duplication followed by rapid protein adaptation to modify signaling specificity, but which continue to trigger conserved developmental programs. Evolutionary constraint is minimized by protein evolution that repurposes developmental modules to enact novel growth characteristics. Finally, in chapter 4, I detail a protocol for efficiently generating reagents for targeted knock-outs of genes, including LRR-RLKs, in maize.
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