Master of Science
Dr. Sangeeta Dhaubhadel
Soybean is one of the most predominantly grown legumes worldwide, however, one deterrent to maximizing its yield is the pathogen, Phytophthora sojae, which causes stem and root rot disease. Many strategies have been implemented to combat this pathogen such as use of pesticides and certain agricultural practices. However, these have been largely ineffective in completely preventing P. sojae infection. An alternative strategy would be to improve the innate resistance of soybean by promoting increased glyceollin production. Glyceollins are soybean-specific antimicrobial agents which are derived from the isoflavonoid branch of the general phenylpropanoid pathway. Soybeans produce 3 forms of glyceollin: glyceollin I, glyceollin II, and glyceollin III that result from the prenylation on either the C-2 or C-4 carbon of glycinol. Currently, only the C4-prenyltransferase (PT) referred to as glycinol 4-dimethylallyltransferase (G4DT), responsible for glyceollin I biosynthesis, has been identified. The objective of the present research is to identify and characterize the isoflavonoid-specific prenyltransferase gene family in soybean. This study has identified a family of 11(iso)flavonoid-specific soybean prenyltransferases (GmPTs) from a total of 63 GmPTs. Nine of these genes were characterized, from which, five were found to be induced upon pathogen infection. These induced GmPTs were shown to localize to plastids and display differential tissue-specific expression. They all contain promoter motifs associated with induction by a broad range of biotic and abiotic stress. In addition, one QTL was found to contain the loci for GmPT01. These findings demonstrate that there is isoflavonoid-specific GmPT family that play a role in glyceollin production.
Sukumaran, Arjun, "Identification and Characterization of the Isoflavonoid-Specific Prenyltransferase Gene Family to Prevent Stem and Root Rot in Soybean" (2016). Electronic Thesis and Dissertation Repository. 4130.
Available for download on Sunday, August 26, 2018