Actin depolymerization is able to increase plant resistance against pathogens via activation of salicylic acid signalling pathway

Hana Leontovyčová,Romana Pospíchalová,Tetiana Kalachova,Kateřina Malínská,Lucie Lamparová,Olga Valentová,Martin Janda,Lenka Burketová,Petre I Dobrev,Lucie Trdá

doi:10.1038/s41598-019-46465-5

Abstract

The integrity of the actin cytoskeleton is essential for plant immune signalling. Consequently, it is generally assumed that actin disruption reduces plant resistance to pathogen attack. Here, we demonstrate that actin depolymerization induced a dramatic increase in salicylic acid (SA) levels in Arabidopsis thaliana. Transcriptomic analysis showed that the SA pathway was activated due to the action of isochorismate synthase (ICS). The effect was also confirmed in Brassica napus. This raises the question of whether actin depolymerization could, under particular conditions, lead to increased resistance to pathogens. Thus, we explored the effect of pretreatment with actin-depolymerizing drugs on the resistance of Arabidopsis thaliana to the bacterial pathogen Pseudomonas syringae, and on the resistance of an important crop Brassica napus to its natural fungal pathogen Leptosphaeria maculans. In both pathosystems, actin depolymerization activated the SA pathway, leading to increased plant resistance. To our best knowledge, we herein provide the first direct evidence that disruption of the actin cytoskeleton can actually lead to increased plant resistance to pathogens, and that SA is crucial to this process.

Highlights

Www.nature.com/scientificreports actin cytoskeleton[6,7]
To establish that salicylic acid (SA) levels can increase upon actin depolymerization, we measured phytohormone content in A. thaliana seedlings treated with just 200 nM latrunculin B
Our results indicate that depolymerized actin can trigger resistance to bacterial or fungal pathogens

Summary

Introduction

Www.nature.com/scientificreports actin cytoskeleton[6,7]. Another effector, HopG1, was shown to affect the remodelling of the actin cytoskeleton in Pst DC3000-infected A. thaliana[11]. In tobacco, cytochalasin E induced the transcription of NtPR-1 (pathogenesis-related 1), a defence-related SA marker gene, and is able to prime cells to HR-like cell death in response to Erysiphe cichoracearum[16]. Both cytochalasin E and latrunculin B induced the transcription of several SA marker genes (AtPR-1, AtPR-2 and AtWRKY38) in A. thaliana seedlings[17]. This suggests that while such drugs do cause actin depolymerization, the effects of such depolymerization may not always be adverse. Could it be that drug-induced actin depolymerization triggers processes that induce the SA pathway and thereby increase plant resistance to pathogens?

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Conclusion