An overview of genetic rust resistance: From broad to specific mechanisms
Race-specific and non–race-specific resistances can be phenotypically quite different (A versus B). (A) Strong resistance is conferred by NLR proteins such as stem rust resistance 45 (Sr45) and is associated with a hypersensitive response. (B) Non–race-specific resistance may be characterised by partial resistance or slowed fungal growth coupled to leaf-tip necrosis in the presence of genes such as leaf rust resistance 67 (Lr67). (C) Adapted pathogens deliver effectors that can subvert pathogen-associated molecular patterns (PAMP)-triggered immunity (PTI), but which may be detected in the plant cell by nucleotide-binding and leucine-rich repeat (NLR) proteins, leading to effector-triggered immunity (ETI). (D) PTI can operate in nonhost resistance in response to nonadapted pathogens, and ETI can also occur for pathogens that are more compatible to the host plant. R-gene capture methods may be used to detect and identify NLR genes, with the goal of incorporation of these NLRs into R-gene cassettes or stacks to provide durable, long-lasting resistance.