Author : Tiffany Marie Lowe-Power
Publisher :
ISBN 13 :
Total Pages : 0 pages
Book Rating : 4.:/5 (18 download)
Book Synopsis Metabolic Analyses of Ralstonia Solanacearum During Plant Pathogenesis by : Tiffany Marie Lowe-Power
Download or read book Metabolic Analyses of Ralstonia Solanacearum During Plant Pathogenesis written by Tiffany Marie Lowe-Power and published by . This book was released on 2017 with total page 0 pages. Available in PDF, EPUB and Kindle. Book excerpt: The bacterial wilt pathogen Ralstonia solanacearum infects host plants through the roots and then systemically colonizes the xylem vessels that transport water and minerals from the roots to shoots. Although xylem sap is dilute and nutrient poor, R. solanacearum thrives in xylem vessels and grows to over 10^9 CFU /g stem. The focus of my thesis research was to investigate metabolic adaptations that enable R. solanacearum success in plant hosts. A previous transcriptomic study found that in tomato xylem, R. solanacearum expresses many catabolic pathways that may contribute to R. solanacearum growth in the xylem, including two pathways that degrade the plant phenolic metabolites, hydroxycinnamic acids and salicylic acid. Hydroxycinnamic acids are plant phenolics that are directly antimicrobial and are also precursors of higher phenolics. To study the role of hydroxycinnamic acid degradation, I created an R. solanacearum mutant lacking the feruloyl-CoA synthase (fcs) that cannot degrade hydroxycinnamic acids. In vitro and in planta experiments with this mutant revealed that hydroxycinnamic acid degradation protected R. solanacearum from the toxicity of two hydroxycinnamic acids, caffeic acid and p-coumaric acid. Further, this catabolic capacity allowed the pathogen to grow on these two metabolites, as well as on the less-toxic ferulic acid. The fcs mutant had delayed growth in tomato roots, which moderately reduced its virulence on tomato plants. Salicylic acid (SA) is a plant defense hormone that primes plants to resist R. solanacearum. I found that expression of the SA degradation pathway was induced by SA itself but not by the pathway intermediate gentisic acid. To determine the role of SA degradation in bacterial wilt disease, I created R. solanacearum mutants that lacked either the first step in SA degradation (nagGH) or the entire pathway (nagAaGHAbIKL). Studies with these mutants demonstrated that SA degradation allowed R. solanacearum to grow on SA, protected the pathogen from SA toxicity, and contributed to R. solanacearum virulence on tobacco but not on tomato plants, which use gentisic acid as a defense signal. My final project used an untargeted metabolomics approach to understand how bacterial wilt disease changes xylem chemistry. I found that bacterial wilt disease increases concentrations of at least eight xylem nutrients that enabled R. solanacearum to grow better in ex vivo sap from infected plants than in sap from healthy plants. This helps explain the rapid growth of this pathogen in host xylem tissue. Second, my work revealed a novel R. solanacearum metabolic virulence strategy: the bacterium produces abundant quantities of the polyamine putrescine in the xylem. Applying exogenous putrescine to tomato plants before inoculation accelerated bacterial growth, bacterial spread, and wilt disease progression. Exogenous putrescine, which is not a bacterial nutrient, facilitated success of diverse R. solanacearum strains on tobacco and three different tomato lines. Moreover, putrescine was also increased in xylem sap of tomato plants infected with a fungal vascular pathogen, suggesting that this polyamine may play a general role in wilt disease development.
