Oomycete small RNAs bind to the plant RNA-induced silencing complex for virulence
Abstract
The exchange of small RNAs (sRNAs) between hosts and pathogens can lead to gene silencing in the recipient organism, a mechanism termed cross-kingdom RNAi (ck-RNAi). While fungal sRNAs promoting virulence are established, the significance of ck-RNAi in distinct plant pathogens is not clear. Here, we describe that sRNAs of the pathogen Hyaloperonospora arabidopsidis, which represents the kingdom of oomycetes and is phylogenetically distant from fungi, employ the host plant's Argonaute (AGO)/RNA-induced silencing complex for virulence. To demonstrate H. arabidopsidis sRNA (HpasRNA) functionality in ck-RNAi, we designed a novel CRISPR endoribonuclease Csy4/GUS reporter that enabled in situ visualization of HpasRNA-induced target suppression in Arabidopsis. The significant role of HpasRNAs together with AtAGO1 in virulence was revealed in plant atago1 mutants and by transgenic Arabidopsis expressing a short-tandem-target-mimic to block HpasRNAs, that both exhibited enhanced resistance. HpasRNA-targeted plant genes contributed to host immunity, as Arabidopsis gene knockout mutants displayed quantitative enhanced susceptibility.
Data availability
Sequencing data have been deposited in NCBI SRA (PRJNA395139).
Article and author information
Author details
Funding
Deutsche Forschungsgemeinschaft (WE 5707/1-1)
- Arne Weiberg
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
Reviewing Editor
- Axel A Brakhage, Hans Knöll Institute, Germany
Version history
- Received: February 17, 2020
- Accepted: May 21, 2020
- Accepted Manuscript published: May 22, 2020 (version 1)
- Accepted Manuscript updated: May 26, 2020 (version 2)
- Version of Record published: June 16, 2020 (version 3)
Copyright
© 2020, Dunker et al.
This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.
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