Submitted to: Plant Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/20/2014
Publication Date: 7/20/2014
Citation: Okubara, P.A., Dickman, M.B., Blechl, A.E. 2014. Molecular and genetic aspects of controlling the soilborne necrotrophic pathogens Rhizoctonia and Pythium. Plant Science. 128:61-70. Interpretive Summary: Biotechnology offers unique and valuable approaches to generating resistance to otherwise hard-to-control soilborne fungal pathogens. Our data indicate that single genes encoding enzymes that degraded pathogen cell walls or inhibitors of plant cell death reduce disease severity ratings from 2.4 to 0.4-0.7, and improve root biomass 30-46%. Leads for biological control systems and from genomics can potentially be deployed for better host protection.
Technical Abstract: The soilborne necrotrophic pathogens Rhizoctonia and Pythium infect a wide range of crops in the US and worldwide. These pathogens pose challenges to growers because the diseases they cause are not adequately controlled by fungicides, rotation or, for many hosts, natural genetic resistance. Although a combination of management practices are likely to be required for control of Rhizoctonia and Pythium, genetic resistance remains a key missing component. This review discusses the recent deployment of introduced genes and genome-based information for control of Rhizoctonia, with emphasis on three pathosystems: Rhizoctonia solani AG8 and wheat, R. solani AG1-IA and rice, and R. solani AG3 or AG4 and potato. Molecular mechanisms underlying disease suppression will be addressed, if appropriate. Although less is known about genes and factors suppressive to Pythium, pathogen genomics and biological control studies are providing useful leads to effectors and antifungal factors. Prospects for resistance to Rhizoctonia and Pythium spp. will continue to improve with growing knowledge of pathogenicity strategies, host defense gene action relative to the pathogen infection process, and the role of environmental factors on pathogen-host interactions.