Study of charcoal rot disease using the model plant Arabidopsis Thaliana
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Macrophomina phaseolina is a warm climate fungal pathogen of the Botryosphaeriaceae family that causes charcoal rot disease in over 700 plant species including commercially grown plants such as soybean, maize, peanut and cotton. Currently used management approaches for the disease including irrigation, addition of organic amendments and crop rotation are not very effective. Limited knowledge on host-pathogen interactions hinders the development of disease resistance strain by genetic engineering. To understand the disease mechanisms at the molecular level, we chose to use Arabidopsis thaliana as a model to study charcoal rot. In this study we established Arabidopsis as a susceptible host for Macrophomina phaseolina. Furthermore, the cellular process of infection and propagation of the pathogen within the host system during the early and late stages of infection were examined by microscopy. Recent studies have demonstrated the crucial roles of different phytohormones in the induction of defense signaling pathways. Here, the interactions between plant hormone-mediated signaling and plant disease resistance were studied using a genetics approach with a hope of understanding the mechanisms of plant immunity against Macrophomina phaseolina mediated by auxin, SA, JA, ET and ABA. In this study we hypothesized that the necrotrophic fungus M. phaseolina invades the host by affecting the biosynthesis of plant hormones (mainly JA, ET and auxin) and/or activation of the corresponding hormonal pathways that are directly or indirectly involved in mounting a defense response against the pathogen. Several mutants that carry mutations in genes that are involved in hormone biosynthesis or signaling were obtained and tested. Results from our study showed that auxin, ET and SA signaling pathways have possible roles of in imparting pathogen resistance against M. phaseolina.
Thesis (M.S.)--Wichita State University, Fairmount College of Liberal Arts and Sciences, Dept. of Biological Sciences.