Laurel wilt is a vascular wilt disease caused by Raffaelea lauricola, a mycangial symbiont of an ambrosia beetle, Xyleborus glabratus. The fungus and vector are native to Asia but were apparently introduced to the Savannah, GA, area 15 or more years ago. Laurel wilt has caused widespread mortality on redbay (Persea borbonia) and other members of the Lauraceae in the southeastern United States, and the pathogen and vector have spread as far as Texas. Although believed to be a single introduction, there has been no extensive study on genetic variation of R. lauricola populations that would suggest a genetic bottleneck in the United States. Ten isolates of R. lauricola from Japan, 55 from Taiwan, and 125 from the United States were analyzed with microsatellite and 28S rDNA markers, and with primers developed for two mating-type genes. The new primers identified isolates as either MAT1 or MAT2 mating types in roughly equal proportions in Taiwan and Japan, where there was also high genetic diversity within populations based on all the markers, suggesting that these populations may have cryptic sex. Aside from a local population near Savannah and a single isolate in Alabama that had unique microsatellite alleles, the U.S. population was genetically uniform and included only the MAT2 mating type, supporting the single introduction hypothesis. This study suggests the importance of preventing a second introduction of R. lauricola to the United States, which could introduce the opposite mating type and allow for genetic recombination.

I have so many people to acknowledge for supporting me in some way on my journey that I cannot list everyone. I thank Chase Mayers, Yeganeh Gharabigloozare, Ashley West, Denise Valdetaro, Cindy Wilkinson, and Douglas McNew for technical assistance. I thank Steve Fraedrich for providing numerous fungal isolates needed for this study and Sheng-Shan Lu for assisting me in collecting precious fungal isolates in Taiwan. I thank Thomas Harrington for taking me on as his student, for always believing in me, and for supporting me to pursue numerous opportunities to broaden my horizons and career experience. I thank my POS committee members, Dennis Lavrov and Leanor Leandro. I give special thanks to Mark Gleason for giving me extra moral support and an office to cry in when I needed it. I thank the department of Plant Pathology and Microbiology faculty and staff for their guidance and support throughout my graduate career at Iowa State. I especially thank Dai Nguyen for applying for my Plant Science Fellowship and her constant encouragement. I thank Chi-Yu Chen, his students at National Taichung University, and the Taiwan Forestry Research Institute for their support. I thank my family and friends, for whom this thesis would not be possible without their endless love and support. I thank Carver Nebbe, my psychiatrist, for his earnest support and helping me to reunite with my intern and emotional support cat, Sammy. I thank Rachel Brenner and Taylor Locker, my therapists at Iowa State, for their support. I thank my colleague, Hafizi Rosli, for his constant encouragement and moral support. I thank my sister, Romana, for empowering me to include the details of my emotional struggles in my thesis and be the most authentic version of myself.