Signalling requirements for Erwinia amylovora-induced disease resistance, callose deposition and cell growth in the non-host Arabidopsis thaliana

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Molecular Plant Pathology - 2017 - Hamdoun - Signalling requirements for Erwinia amylovora‐induced disease resistance.pdf (983.29 KB)

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 http://hdl.handle.net/11603/24708

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https://orcid.org/0000-0002-7496-3200

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2017-07-29

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journal articles
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Hamdoun, S., Gao, M., Gill, M., Kwon, A., Norelli, J.L. and Lu, H. (2018), Signalling requirements for Erwinia amylovora-induced disease resistance, callose deposition and cell growth in the non-host Arabidopsis thaliana. Molecular Plant Pathology, 19: 1090-1103. https://doi.org/10.1111/mpp.12588

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This work was written as part of one of the author's official duties as an Employee of the United States Government and is therefore a work of the United States Government. In accordance with 17 U.S.C. 105, no copyright protection is available for such works under U.S. Law.
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Abstract

Erwinia amylovora is the causal agent of the fire blight disease in some plants of the Rosaceae family. The non-host plant Arabidopsis serves as a powerful system for the dissection of mechanisms of resistance to E. amylovora. Although not yet known to mount gene-for-gene resistance to E. amylovora, we found that Arabidopsis activated strong defence signalling mediated by salicylic acid (SA), with kinetics and amplitude similar to that induced by the recognition of the bacterial effector avrRpm1 by the resistance protein RPM1. Genetic analysis further revealed that SA signalling, but not signalling mediated by ethylene (ET) and jasmonic acid (JA), is required for E. amylovora resistance. Erwinia amylovora induces massive callose deposition on infected leaves, which is independent of SA, ET and JA signalling and is necessary for E. amylovora resistance in Arabidopsis. We also observed tumour-like growths on E. amylovora-infected Arabidopsis leaves, which contain enlarged mesophyll cells with increased DNA content and are probably a result of endoreplication. The formation of such growths is largely independent of SA signalling and some E. amylovora effectors. Together, our data reveal signalling requirements for E. amylovora-induced disease resistance, callose deposition and cell fate change in the nonhost plant Arabidopsis. Knowledge from this study could facilitate a better understanding of the mechanisms of host defence against E. amylovora and eventually improve host resistance to the pathogen.