Abstract
Because of their sessile nature, plants evolved integrated defense and acclimation mechanisms to simultaneously cope with adverse biotic and abiotic conditions. Among these are systemic acquired resistance (SAR) and systemic acquired acclimation (SAA). Growing evidence suggests that SAR and SAA activate similar cellular mechanisms and employ common signaling pathways for the induction of acclimatory and defense responses. It is therefore possible to consider these processes together, rather than separately, as a common systemic acquired acclimation and resistance (SAAR) mechanism. Arabidopsis thaliana flavin-dependent monooxygenase 1 (FMO1) was previously described as a regulator of plant resistance in response to pathogens as an important component of SAR. In the current study, we investigated its role in SAA, induced by a partial exposure of Arabidopsis rosette to local excess light stress. We demonstrate here that FMO1 expression is induced in leaves directly exposed to excess light stress as well as in systemic leaves remaining in low light. We also show that FMO1 is required for the systemic induction of ASCORBATE PEROXIDASE 2 (APX2) and ZINC-FINGER OF ARABIDOPSIS 10 (ZAT10) expression and spread of the reactive oxygen species (ROS) systemic signal in response to a local application of excess light treatment. Additionally, our results demonstrate that FMO1 is involved in the regulation of excess light-triggered systemic cell death, which is under control of LESION SIMULATING DISEASE 1 (LSD1). Our study indicates therefore that FMO1 plays an important role in triggering SAA response, supporting the hypothesis that SAA and SAR are tightly connected and use the same signaling pathways.
Highlights
Because of their sessile nature, in the course of evolution plants have evolved systemic defense mechanisms in response to many different stresses, including pathogens, wounding and abiotic stresses, which are essential for plant survival in unfavorable conditions
To test whether the flavin-dependent monooxygenase 1 (FMO1) gene is induced upon Excess Light (EL) treatment in local (LL) and/or untreated leaves we performed a time-course quantitative polymerase chain reaction (PCR) (qPCR) analysis for non-treated, as well as EL-treated, local leaves and systemic leaves remaining in low light
Our results indicated that FMO1 expression was induced, not statistically significantly, both locally and systemically already after the 2 min long EL treatment (Figure 1)
Summary
Because of their sessile nature, in the course of evolution plants have evolved systemic defense mechanisms in response to many different stresses, including pathogens, wounding and abiotic stresses, which are essential for plant survival in unfavorable conditions. One of these mechanisms is systemic acquired resistance (SAR), in which, upon local pathogen attack, plants induce protection against a subsequent infection, leading to broad-spectrum disease resistance at distal, uninfected tissues. High-light treatment is able to induce specific changes in the bundle sheath parenchyma cells plasma membrane electrical potential, called photoelectrophysiological signaling (PEPS) and physical interruption of bundle sheath cells layer blocked PEPS and SAA induction [10]. In Arabidopsis thaliana, robust molecular markers of SAA, ASCORBATE PEROXIDASE 2 (APX2, AT3G09640) and ZINC-FINGER OF ARABIDOPSIS 10
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