Abstract:
Eucalyptus grandis, in its native Australian range, varies in resistance to Austropuccinia
psidii (syn. Puccinia psidii). The biotrophic rust fungus, A. psidii is the causal agent
of myrtle rust and poses a serious threat to Australian biodiversity. The pathogen
produces yellow pustules of urediniospores on young leaves and shoots, resulting in
shoot tip dieback, stunted growth, and death. Dissecting the underlying mechanisms
of resistance against this pathogen will contribute to improved breeding and control
strategies to mitigate its devastating effects. The aim of this study was to determine
the molecular dialogue between E. grandis and A. psidii, using an RNA-sequencing
approach. Resistant and susceptible E. grandis seedlings grown from seed collected
across its natural range were inoculated with the pandemic biotype of A. psidii. The leaf
tissue was harvested at 12-h post inoculation (hpi), 1-day post inoculation (dpi), 2-dpi
and 5-dpi and subjected to RNA-sequencing using Illumina 50 bp PE reads to a depth of
40 million reads per sample. Differential gene expression and gene ontology enrichment
indicated that the resistant seedlings showed controlled, coordinated responses with a
hypersensitive response, while the susceptible seedlings showed no systemic response
against myrtle rust. Brassinosteroid signaling was apparent as an enriched term in
the resistant interaction at 2-dpi, suggesting an important role of this phytohormone
in defense against the pathogen. Brassinosteroid mediated signaling genes were also
among the candidate genes within two major disease resistance loci (Puccinia psidii
resistance), Ppr3 and Ppr5. While brassinosteroids have been tagged as positive
regulators in other plant disease resistance interactions, this is the first report in the
Eucalyptus – Austropuccinia psidii interaction. Furthermore, several putative resistance genes, underlying known resistance loci and implicated in the interaction have been
identified and highlighted for future functional studies. This study provided further
insights into the molecular interactions between E. grandis and A. psidii, contributing
to our understanding of this pathosystem.
