No abstract

The Rdm4 gene from soybean cv. Hutcheson has been extensively used to incorporate resistance to soybean stem canker (SSC), caused by Diaporthe phaseolorum var. meridionalis (Dpm), into soybean commercial cultivars. The objective of this work was to characterize the inheritance of the Rdm4 locus in different populations derived from the cross: J77-339 (rdm ⁄ rdm, susceptible) · Hutcheson (Rdm4 ⁄ Rdm4, resistant) in independent interactions with two local isolates of Dpm. Four F 2 populations were obtained and two were advanced to the F 3 generation as separate F 2:3 families to perform progeny tests. Each population was inoculated with the CE109 and ⁄ or CE112 isolates of Dpm. Within each plant-pathogen interaction, the resistance gene segregated as completely dominant. However, cross resistance, or opposite disease reactions, to CE109 and CE112 isolates of Dpm were observed in four F 2:3 families, indicating an intergenic recombination event between two nonallelic genes interacting specifically with each isolate of Dpm. The distance between them, estimated as the recombination fraction, was 29%, suggesting that both genes were not tightly linked, but close enough to segregate together in most crosses. Results indicated the existence of a genomic region in cv. Hutcheson composed of race-specific resistance loci with at least two Rdm genes: the previously recognized Rdm4 and a novel gene, tentatively named Rdm5, conferring specific resistance to Dpm isolates CE109 and CE112.

Xanthomonas citri ssp. citri (X. citri) is the causal agent of Asiatic citrus canker, a disease that seriously affects most commercially important Citrus species worldwide. We have identified previously a natural variant, X. citri A , that triggers a host-specific defence response in Citrus limon. However, the mechanisms involved in this canker disease resistance are unknown. In this work, the defence response induced by X. citri A was assessed by transcriptomic, physiological and ultrastructural analyses, and the effects on bacterial biofilm formation were monitored in parallel. We show that X. citri A triggers a hypersensitive response associated with the interference of biofilm development and arrest of bacterial growth in C. limon. This plant response involves an extensive transcriptional reprogramming, setting in motion cell wall reinforcement, the oxidative burst and the accumulation of salicylic acid (SA) and phenolic compounds. Ultrastructural analyses revealed subcellular changes involving the activation of autophagy-associated vacuolar processes. Our findings show the activation of SA-dependent defence in response to X. citri A and suggest a coordinated regulation between the SA and flavonoid pathways, which is associated with autophagy mechanisms that control pathogen invasion in C. limon. Furthermore, this defence response protects C. limon plants from disease on subsequent challenges by pathogenic X. citri. This knowledge will allow the rational exploitation of the plant immune system as a biotechnological approach for the management of the disease.