Understanding Host-Fungus Interactions between Soybean and Phakopsora pachyrhizi to Enhance Soybean Resistance to Rust Disease

Abstract

Asian soybean rust (ASR) caused by Phakopsora pachyrhizi was first reported in Japan in 1902. In 2004, Asian soybean rust was first reported in Louisiana and other Southeastern US states. It is one of the most important soybean diseases worldwide. Even though fungicide application can offer some protection and prevent severe yield losses caused by ASR if applied promptly, it is not a viable option as a long-term disease control measure because it increases the growers’ operation costs and the risk of environmental pollution. In addition, it also increases the chances of developing fungicide resistance within a pathogen population. The exact soybean rust resistance mechanism is poorly understood/or investigated, which makes the effort of developing rust resistant commercial soybean lines a challenge. In this dissertation, soybean rust resistance mechanism and novel soybean rust disease control methods are explored. The direct involvement of 4 differentially expressed P. pachyrhizi infection-induced proteins (PR10, CHI, APX, and GOX) identified in previous proteomics studies in soybean resistance to P. pachyrhizi infection was demonstrated using a bean pod mottle virus (BPMV) based virus induced gene silencing (VIGS) approach. Besides compromising ASR resistance, pr10-silenced plants grew shorter, had smaller soybean leaf size, and generated less ROS, which suggests that PR10 is also involved in plant growth and development. To increase our chance of identifying genes or proteins that are directly involved in soybean resistance to P. pachyrhizi infection, a pair of recombinant inbred lines (RILs) of ASR-susceptible (94a) and ASR-resistant (94c) soybean lines with similar genetic background were used to investigate the soybean basal and inducible defense mechanisms in response to P. pachyrhizi through histological study and analyzing differentially expressed genes between RILs with and without rust inoculation. The presence of wax crystals may prevent a close interaction of appressoria with the leaf surface and mask its recognition by the pathogen, or certain chemical compounds may be missing on the leaf surface of 94c that are required for recognition during initial penetration. ROS production at the site of infection and the thicker cuticle layer caused appressorium rupture and might also contribute to longer germ tube growth. A HIGS approach that is similar to BPMV-based VIGS demonstrated that double-stranded RNAs (dsRNAs) of P. pachyrhizi genes can be used to suppress the expression of targeted fungal genes resulting in reduced pathogen infection and disease severity. In addition, direct spraying of double-stranded RNAs (dsRNAs) targeting an acetyl-CoA acyltransferase (ATC), a