Abstract

Sudden death syndrome (SDS) of soybean is a complex root rot disease caused by the semi-biotrophic fungus Fusarium solani (F. solani) and a leaf scorch disease; caused by toxins produced by pathogen in the roots. However, the mechanism of soybean resistant to F. solani is still poorly understood. Eighteen soybean cultivars were screened for SDS resistance, with one cultivar showing susceptibility and one cultivar showing resistance to F. solani infection. Histochemical analysis with diaminobenzidine (DAB) and Trypan blue staining indicated an accumulation of reactive oxygen species (ROS) and cell death in surrounding area of SDS which was higher in susceptible cultivar than in resistant cultivar. Furthermore, exogenous salicylic acid (SA) application also induced some level of resistance to F. solani by the susceptible cultivar. A biochemical study revealed that the activities of superoxide dismutase (SOD), peroxidase (POD), and enzymes involved in scavenging ROS, increased in susceptible cultivar after SDS infection. In addition, hydrogen peroxide (H₂O₂) and malondialdehyde (MDA) content also increased in the susceptible cultivar than in resistant cultivar. High-performance liquid chromatography (HPLC) analysis indicated that free and total salicylic acid (SA) content increased in the susceptible cultivar than in resistant cultivar. In addition, a real-time quantitative PCR analysis showed an accumulation of pathogen related (PR) genes in the resistant cultivar than in susceptible cultivar. Our results show that (i). F. solani infection can increase endogenous SA levels, antioxidase activities, ROS and cell death in susceptible soybean cultivar to induce resistance against Fusarium solani. (ii). F. solani infection induced the expression of SA marker genes in resistant soybean cultivar to enhance resistance.

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