Botrytis cinerea manipulates the antagonistic effects between immune pathways to promote disease development in tomato.

Mohamed El Oirdi,Fouad Daayf,Kamal Bouarab,Taha Abd El Rahman,Abdelbasset El Hadrami,María Cecilia Rodriguez,Adrian Vojnov,Luciano Rigano

doi:10.1105/tpc.111.083394

Abstract

Plants have evolved sophisticated mechanisms to sense and respond to pathogen attacks. Resistance against necrotrophic pathogens generally requires the activation of the jasmonic acid (JA) signaling pathway, whereas the salicylic acid (SA) signaling pathway is mainly activated against biotrophic pathogens. SA can antagonize JA signaling and vice versa. Here, we report that the necrotrophic pathogen Botrytis cinerea exploits this antagonism as a strategy to cause disease development. We show that B. cinerea produces an exopolysaccharide, which acts as an elicitor of the SA pathway. In turn, the SA pathway antagonizes the JA signaling pathway, thereby allowing the fungus to develop its disease in tomato (Solanum lycopersicum). SA-promoted disease development occurs through Nonexpressed Pathogen Related1. We also show that the JA signaling pathway required for tomato resistance against B. cinerea is mediated by the systemin elicitor. These data highlight a new strategy used by B. cinerea to overcome the plant's defense system and to spread within the host.

Highlights

Plants fight microbial attacks using both constitutive and induced defenses, which include basal and highly specific resistance (Jones and Dangl, 2006)
B. cinerea–Tomato Interaction Pathogenicity tests were performed on tomato (S. lycopersicum cv Moneymaker) leaves inoculated with two isolates of B. cinerea, B191 and B8403
These results suggest that jasmonic acid (JA) signaling is involved in tomato resistance to B. cinerea isolate B8403, which is consistent with previous reports (AbuQamar et al, 2008)

Summary

Introduction

Plants fight microbial attacks using both constitutive and induced defenses, which include basal and highly specific resistance (Jones and Dangl, 2006). 2406 The Plant Cell activated by the biotroph suppressed the level of JA-dependent resistance against the necrotroph (Spoel et al, 2007). Pseudomonas syringae produces the phytotoxin coronatine, which functions as a JA mimic and suppresses SA-dependent defenses, thereby promoting susceptibility of the plant to this pathogen (Brooks et al, 2005; Cui et al, 2005; Glazebrook, 2005; Laurie-Berry et al, 2006). Simultaneous activation of SA- and JA-dependent defense pathways resulted in enhanced resistance to pathogenic P. syringae pv tomato DC3000 compared with either pathway-related defense response alone (van Wees et al, 2000; O’Donnell et al, 2003). Nonexpressed Pathogen Related (NPR1) was shown to be a key regulator of SA-mediated suppression of JA signaling (Spoel et al, 2003; Ndamukong et al, 2007)

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Conclusion