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FMO1 Is Involved in Excess Light Stress-Induced Signal Transduction and Cell Death Signaling

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 acti...

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Autores principales: Czarnocka, Weronika, Fichman, Yosef, Bernacki, Maciej, Różańska, Elżbieta, Sańko-Sawczenko, Izabela, Mittler, Ron, Karpiński, Stanisław
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7600522/
https://www.ncbi.nlm.nih.gov/pubmed/32987853
http://dx.doi.org/10.3390/cells9102163
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author Czarnocka, Weronika
Fichman, Yosef
Bernacki, Maciej
Różańska, Elżbieta
Sańko-Sawczenko, Izabela
Mittler, Ron
Karpiński, Stanisław
author_facet Czarnocka, Weronika
Fichman, Yosef
Bernacki, Maciej
Różańska, Elżbieta
Sańko-Sawczenko, Izabela
Mittler, Ron
Karpiński, Stanisław
author_sort Czarnocka, Weronika
collection PubMed
description 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.
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spelling pubmed-76005222020-11-01 FMO1 Is Involved in Excess Light Stress-Induced Signal Transduction and Cell Death Signaling Czarnocka, Weronika Fichman, Yosef Bernacki, Maciej Różańska, Elżbieta Sańko-Sawczenko, Izabela Mittler, Ron Karpiński, Stanisław Cells Article 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. MDPI 2020-09-24 /pmc/articles/PMC7600522/ /pubmed/32987853 http://dx.doi.org/10.3390/cells9102163 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Czarnocka, Weronika
Fichman, Yosef
Bernacki, Maciej
Różańska, Elżbieta
Sańko-Sawczenko, Izabela
Mittler, Ron
Karpiński, Stanisław
FMO1 Is Involved in Excess Light Stress-Induced Signal Transduction and Cell Death Signaling
title FMO1 Is Involved in Excess Light Stress-Induced Signal Transduction and Cell Death Signaling
title_full FMO1 Is Involved in Excess Light Stress-Induced Signal Transduction and Cell Death Signaling
title_fullStr FMO1 Is Involved in Excess Light Stress-Induced Signal Transduction and Cell Death Signaling
title_full_unstemmed FMO1 Is Involved in Excess Light Stress-Induced Signal Transduction and Cell Death Signaling
title_short FMO1 Is Involved in Excess Light Stress-Induced Signal Transduction and Cell Death Signaling
title_sort fmo1 is involved in excess light stress-induced signal transduction and cell death signaling
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7600522/
https://www.ncbi.nlm.nih.gov/pubmed/32987853
http://dx.doi.org/10.3390/cells9102163
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