Genomic and Effector‐Based Insights Into Austropuccinia psidii–Host Interactions Informing RNAi and Resistance Development

TL;DR

This paper explores the genome and effectors of the myrtle rust pathogen to develop RNAi treatments and improve resistance in host plants.

Contribution

The study provides insights into the large A. psidii genome and its effectors, offering new targets for RNAi and resistance strategies.

Findings

The A. psidii genome is one of the largest fungal genomes, with a haploid size of 1 gigabase.

Early-expressed effectors in A. psidii are potential targets for RNAi-based disease control.

RNAi targeting effectors has shown promise in laboratory and greenhouse experiments.

Abstract

Austropuccinia psidii is a biotrophic basidiomycete and the causal pathogen of myrtle rust. The pandemic biotype infects over 480 Myrtaceae species and has caused functional extinction of myrtaceous species on the east coast of Australia, threatening numerous others worldwide. In planta resistance has been extensively explored, and resistant phenotypes are used in breeding programmes. At a molecular level, loci conferring resistance and secondary metabolite pathways activated during infection are being defined. A key component necessary to investigate this plant–pathogen interaction is an assembled and annotated pathogen genome. The A. psidii genome, determined to be one of the largest fungal genomes assembled to date, has a haploid size of 1 gigabase. Many putative effector sequences are present in the A. psidii genome: effectors are relatively small proteins that have been shown in other pathogen–host systems to facilitate infection through manipulation of the host's cellular processes. Some A. psidii effectors are expressed early during urediniospore germination and initial invasion of plant tissues, and thus may be unique targets for pathogen control. For example, in vitro RNA interference (RNAi) targeting the expression of A. psidii effector proteins for disease control has been demonstrated in laboratory and green/glasshouse experiments, but has yet to be tested in situ. Emerging host genomes and the characterisation of A. psidii effectors will continue to shed light on A. psidii–host interactions, aiding in the creation or optimisation of new treatments. Alternatively, treatments such as nanobodies or synthetic decoy resistance proteins could provide new means of disease prevention.

Genomic and effector‐based insights into Austropuccinia psidii—host interactions are informing RNAi treatments and aiding resistance development for myrtle rust disease.

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