Abstract
Reactive oxygen species (ROS) play a central role in plant immune responses. The most important virulence factors of the Stagonospora nodorum Berk. are multiple fungal necrotrophic effectors (NEs) (SnTox) that affect the redox-status and cause necrosis and/or chlorosis in wheat lines possessing dominant susceptibility genes (Snn). However, the effect of NEs on ROS generation at the early stages of infection has not been studied. We studied the early stage of infection of various wheat genotypes with S nodorum isolates -Sn4VD, SnB, and Sn9MN, carrying a different set of NE genes. Our results indicate that all three NEs of SnToxA, SnTox1, SnTox3 significantly contributed to cause disease, and the virulence of the isolates depended on their differential expression in plants (Triticum aestivum L.). The Tsn1–SnToxA, Snn1–SnTox1and Snn3–SnTox3 interactions played an important role in inhibition ROS production at the initial stage of infection. The Snn3–SnTox3 inhibited ROS production in wheat by affecting NADPH-oxidases, peroxidases, superoxide dismutase and catalase. The Tsn1–SnToxA inhibited ROS production in wheat by affecting peroxidases and catalase. The Snn1–SnTox1 inhibited the production of ROS in wheat by mainly affecting a peroxidase. Collectively, these results show that the inverse gene-for gene interactions between effector of pathogen and product of host sensitivity gene suppress the host’s own PAMP-triggered immunity pathway, resulting in NE-triggered susceptibility (NETS). These results are fundamentally changing our understanding of the development of this economical important wheat disease.
Highlights
Introduction published maps and institutional affilPlants have developed several levels of defense against microbial pathogens, which have been described in the “zig-zag” model of the plant immune system [1]
The first line of defense in plants is through the perception of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs), which leads to development of basal immunity, known as PAMP-triggered immunity (PTI) [1]
Obtained results indicate that all three necrotrophic effectors (NEs) of S. nodorum SnToxA, SnTox1, SnTox3 played an important role in inhibition of reactive oxygen species (ROS) during PTI at the initial stage of infection, despite the fact that at the late stage of infection, all three NEs caused the formation of necrosis and chlorosis on wheat leaves of susceptible genotypes
Summary
Introduction published maps and institutional affilPlants have developed several levels of defense against microbial pathogens, which have been described in the “zig-zag” model of the plant immune system [1]. The first line of defense in plants is through the perception of pathogen-associated molecular patterns (PAMPs) by pattern recognition receptors (PRRs), which leads to development of basal immunity, known as PAMP-triggered immunity (PTI) [1]. The pathogen can suppress PTI using effectors which leads to the development of effector-triggered susceptibility (ETS). The second line of defense in plants is called effector-triggered immunity (ETI) and develops when an effector is recognized by products of effector-specific resistance genes, the most common being the so-called nucleotide-binding and leucine-rich repeat domain proteins (NB-LRR class) [1]. The development of PTI and ETI induces similar responses in plants: both lines of defense can be separated in time and space, but both are closely related to the production of reactive oxygen species (ROS) [2].
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