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The plant hypersensitive response (HR), a rapid cell death at the point of pathogenesis, is mediated by nucleotide‐binding site, leucine‐rich repeat (NLR) resistance proteins (R‐proteins) that recognize the presence of specific pathogen‐derived proteins. Rp1‐D21 is an autoactive maize NLR R‐protein that triggers HR spontaneously. We previously mapped loci associated with variation in the strength of HR induced by Rp1‐D21. Here we identify the E3 ligase  ZmMIEL1  as the causal gene at a chromosome 10 modifier locus. Transient  ZmMIEL1  expression in  Nicotiana benthamiana  reduced HR induced by Rp1‐D21, while suppression of  ZmMIEL1  expression in maize carrying  Rp1‐D21  increased HR. ZmMIEL1 also suppressed HR induced by another autoactive NLR, the  Arabidopsis  R‐protein RPM1D505V, in  N. benthamiana . We demonstrated that ZmMIEL1 is a functional E3 ligase and that the effect of ZmMIEL1 was dependent on the proteasome but also that levels of Rp1‐D21 and RPM1D505V were not reduced when coexpressed with ZmMIEL1 in the  N. benthamiana  system. By comparison to a similar system in  Arabidopsis , we identify ZmMYB83 as a potential target of ZmMIEL1. Suppression of  ZmMYB83  expression in maize lines carrying  Rp1‐D21  suppressed HR. Suppression of  ZmMIEL1  expression caused an increase in  ZmMYB83  transcript and protein levels in  N. benthamiana  and maize. Using coimmunoprecipitation and bimolecular fluorescence complementation assays, we demonstrated that ZmMIEL1 and ZmMYB83 physically interacted. Additionally,  ZmMYB83  and  ZmMIEL1  regulated the expression of a set of maize very long chain fatty acid (VLCFA) biosynthetic genes that may be involved in regulating HR.

The maize ZmMIEL1 E3 ligase and ZmMYB83 transcription factor proteins interact and regulate the hypersensitive defence response