A Homolog of the Gene Is Involved in Nonhost Resistance to Wheat Stem Rust in .

Plants resist infection by pathogens using both preexisting barriers and inducible defense responses. Inducible responses are governed in a complex manner by various hormone signaling pathways. The relative contribution of hormone signaling pathways to nonhost resistance to pathogens is not well understood. In this study, we examined the molecular basis of disrupted nonhost resistance to the fungal species , which causes stem rust of wheat, in an induced mutant of the model grass . Through bioinformatic analysis, a 1-bp deletion in the mutant genotype was identified that introduces a premature stop codon in the gene , which is a homolog of the gene (). In , is central to the regulation of the circadian clock and plays a crucial role in jasmonate signaling by attenuating levels of the transcription factor protein MYC2, and its mutational disruption results in enhanced susceptibility to the hemibiotroph . Our similar finding for an obligate biotroph suggests that the biochemical role of in mediating disease resistance to biotrophs is conserved in grasses, and that the correct modulation of jasmonate signaling during infection by may be essential for nonhost resistance to wheat stem rust in .[Formula: see text] Copyright © 2021 The Author(s). This is an open access article distributed under the CC BY 4.0 International license.