An apoplastic peptide signal activates salicylic acid signalling in maize

Ziemann, Sebastian, van der Linde, Karina, Lahrmann, Urs, Acar, Beyda, Kaschani, Farnusch, Colby, Tom, Kaiser, Markus, Ding, Yezhang, Schmelz, Eric, Huffaker, Alisa, Holton, Nicholas, Zipfel, Cyril and Doehlemann, Gunther (2018) An apoplastic peptide signal activates salicylic acid signalling in maize. Nature Plants, 4. 172–180. ISSN 2055-026X

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Abstract

Control of plant pathogen resistance or susceptibility largely depends on the promotion of either cell survival or cell death. In this context, papain-like cysteine proteases (PLCPs) regulate plant defence to drive cell death and protection against biotrophic pathogens. In maize (Zea mays), PLCPs are crucial in the orchestration of salicylic acid (SA)-dependent defence signalling. Despite this central role in immunity, it remains unknown how PLCPs are activated, and which downstream signals they induce to trigger plant immunity. Here, we present the discovery of an immune signalling peptide, Zea mays immune signalling peptide 1 (Zip1). A mass spectrometry approach identified the Zip1 peptide being produced after salicylic acid (SA) treatment. In vitro studies using recombinant proteins demonstrate that PLCPs are required to release bioactive Zip1 from its propeptide precursor (PROZIP1). Strikingly, Zip1 treatment strongly elicits SA accumulation in maize leaves. Moreover, RNAseq based transcriptome analyses revealed that Zip1 and SA treatments induce highly overlapping transcriptional changes. Consequently, Zip1 promotes the infection of the necrotrophic pathogen Botrytis cinerea in maize, while it reduces virulence of the biotrophic fungus Ustilago maydis. Together, Zip1 represents the previously missing signal that is released by PLCPs to activate SA defence signalling.

Item Type: Article
Faculty \ School: Faculty of Science > School of Biological Sciences
Depositing User: Pure Connector
Date Deposited: 06 Mar 2018 16:30
Last Modified: 31 Oct 2020 00:53
URI: https://ueaeprints.uea.ac.uk/id/eprint/66443
DOI: 10.1038/s41477-018-0116-y

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