FMO1 Is Involved in Excess Light Stress-Induced Signal Transduction and Cell Death Signaling.
Weronika CzarnockaYosef FichmanMaciej BernackiElżbieta RóżańskaIzabela Sańko-SawczenkoRon MittlerStanisław KarpińskiPublished in: Cells (2020)
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.
Keyphrases
- cell death
- stress induced
- reactive oxygen species
- arabidopsis thaliana
- transcription factor
- signaling pathway
- poor prognosis
- drug induced
- oxidative stress
- high resolution
- multidrug resistant
- binding protein
- diabetic rats
- cell cycle arrest
- gram negative
- high glucose
- long non coding rna
- smoking cessation
- endoplasmic reticulum stress
- replacement therapy