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The common rust disease of maize is caused by the obligate biotrophic fungusPuccinia sorghi. The maizeRp1-Dallele imparts resistance against theP.sorghiIN2 isolate by initiating a defense response that includes a rapid localized programmed cell death process, the hypersensitive response (HR). In this study, to identify AvrRp1-D fromP.sorghiIN2, we employed the isolation of haustoria, facilitated by a biotin-streptavidin interaction, as a powerful approach. This method proves particularly advantageous in cases where the genome information for the fungal pathogen is unavailable, enhancing our ability to explore and understand the molecular interactions between maize andP.sorghi. The haustorial transcriptome generated through this technique, in combination with bioinformatic analyses such as SignalP and TMHMM, enabled the identification of 251 candidate effectors. We ultimately identified two closely related genes,AvrRp1-D.1andAvrRp1-D.2, which triggered anRp1-D-dependent defense response inNicotiana benthamiana.AvrRp1-D-inducedRp1-D-dependent HR was further confirmed in maize protoplasts. We demonstrated that AvrRp1-D.1 interacts directly and specifically with the leucine-rich repeat (LRR) domain of Rp1-D through yeast two-hybrid assay. We also provide evidence that, in the absence of Rp1-D, AvrRp1-D.1 plays a role in suppressing the plant immune response. Our research provides valuable insights into the molecular interactions driving resistance against common rust in maize. 

Summary The molecular mechanisms of quantitative resistance (QR) to fungal pathogens and their relationships with growth pathways are poorly understood.We identified tomato TRK1 (TPK1b Related Kinase1) and determined its functions in tomato QR and plant growth. TRK1 is a receptor‐like cytoplasmic kinase that complexes with tomato LysM Receptor Kinase (SlLYK1).SlLYK1andTRK1are required for chitin‐induced fungal resistance, accumulation of reactive oxygen species, and expression of immune response genes. Notably, TRK1 and SlLYK1 regulate SlMYC2, a major transcriptional regulator of jasmonic acid (JA) responses and fungal resistance, at transcriptional and post‐transcriptional levels.Further, TRK1 is also required for maintenance of proper meristem growth, as revealed by the ectopic meristematic activity, enhanced branching, and altered floral structures inTRK1RNAi plants. Consistently, TRK1 interacts with SlCLV1 and SlWUS, andTRK1RNAi plants show increased expression ofSlCLV3andSlWUSin shoot apices. Interestingly, TRK1 suppresses chitin‐induced gene expression in meristems but promotes expression of the same genes in leaves. SlCLV1 and TRK1 perform contrasting functions in defense but similar functions in plant growth.Overall, through molecular and biochemical interactions with critical regulators, TRK1 links upstream defense and growth signals to downstream factor in fungal resistance and growth homeostasis response regulators.