Abstract
The production of reactive oxygen species (ROS) is one of the first defense reactions induced in Arabidopsis in response to infection by the pectinolytic enterobacterium Dickeya dadantii. Previous results also suggest that abscisic acid (ABA) favors D. dadantii multiplication and spread into its hosts. Here, we confirm this hypothesis using ABA-deficient and ABA-overproducer Arabidopsis plants. We investigated the relationships between ABA status and ROS production in Arabidopsis after D. dadantii infection and showed that ABA status modulates the capacity of the plant to produce ROS in response to infection by decreasing the production of class III peroxidases. This mechanism takes place independently of the well-described oxidative stress related to the RBOHD NADPH oxidase. In addition to this weakening of plant defense, ABA content in the plant correlates positively with the production of some bacterial virulence factors during the first stages of infection. Both processes should enhance disease progression in presence of high ABA content. Given that infection increases transcript abundance for the ABA biosynthesis genes AAO3 and ABA3 and triggers ABA accumulation in leaves, we propose that D. dadantii manipulates ABA homeostasis as part of its virulence strategy.
Highlights
Abscisic acid (ABA) is well-known as the major phytohormone accumulating in response to abiotic stress such as drought, salt, osmotic or cold stresses, and is involved in plant adaptation to these unfavorable conditions (Nambara and Marion-Poll, 2005)
We have previously shown that abscisic acid (ABA) hypersensitive mutants of Arabidopsis exhibit an increased susceptibility to D. dadantii indicating a role for ABA in the Arabidopsis resistance response (Plessis et al, 2011)
Siderophores secreted into leaf tissues modify the salicylic acid (SA) and jasmonic acid (JA)-related defense responses (Dellagi et al, 2009; Aznar et al, 2014) and unknown bacterial signals lower the oxidative stress (Kraepiel et al, 2011)
Summary
Abscisic acid (ABA) is well-known as the major phytohormone accumulating in response to abiotic stress such as drought, salt, osmotic or cold stresses, and is involved in plant adaptation to these unfavorable conditions (Nambara and Marion-Poll, 2005). When faced with multiple stresses, plants have to prioritize their adaptive responses and, in many cases, ABA promotes abiotic stress responses at the expense of defense reactions to pathogens (Robert-Seilaniantz et al, 2007). ABA promotes stomatal pre-invasive resistance to foliar bacterial pathogens (Melotto et al, 2006) and stimulates callose accumulation in papillae in response to the fungal necrotrophic pathogen Leptosphaeria maculens (Ton et al, 2009; Cao et al, 2011). ABA exhibits contrasted roles in plant defense depending on infection phase and pathogen lifestyle. This highlights the importance of studying each interaction and its kinetics individually
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