HsfA1a is essential for Mi-1.2-mediated resistance to Meloidogyne incognita, and regulates Wfi1 transcription and H2O2 production

Plants generate reactive oxygen species (ROS) in the apoplast in response to pathogen attack, especially following resistance ( R ) gene-mediated pathogen recognition; however, the mechanisms activating ROS generation remain unknown. Here, we demonstrate that RKN ( Meloidogyne incognita ) infection rapidly induces ROS accumulation in the roots of tomato ( Solanum lycopersicum ) plants that contain the R gene Mi-1.2 but rarely induces ROS accumulation in the susceptible or Mi-1.2 -silenced resistant genotypes. RNK also induces the hypersensitive response, a form of programmed cell death, in Mi-1.2 plants. RKN induces the expression of numerous class-A heat shock factor (HsfA) genes in resistant tomato plants. Silencing HsfA1a compromises Mi-1.2 -mediated resistance, apoplastic H 2 O 2 accumulation, and the transcription of whitefly induced 1 ( Wfi1 ), which encodes a respiratory burst oxidase homolog. HsfA1a regulates Wfi1 transcription by binding to the Wfi1 promoter, and silencing of Wfi1 compromises Mi-1.2 -mediated resistance. HsfA1a and Wfi1 are involved in Mi-1.2-triggered Hsp90 accumulation and basal defense in susceptible tomato. Thus, HsfA–1aWfi1-dependent ROS signaling functions as a crucial regulator of plant defense responses.