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OXR2 Increases Plant Defense against a Hemibiotrophic Pathogen via the Salicylic Acid Pathway

Arabidopsis ( ) OXIDATION RESISTANCE2 (AtOXR2) is a mitochondrial protein belonging to the Oxidation Resistance (OXR) protein family, recently described in plants. We analyzed the impact of AtOXR2 in Arabidopsis defense mechanisms against the hemibiotrophic bacterial pathogen mutant plants are more...

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Bibliographic Details
Published in:Plant physiology (Bethesda) 2020-10, Vol.184 (2), p.1112-1127
Main Authors: Mencia, Regina, Céccoli, Gabriel, Fabro, Georgina, Torti, Pablo, Colombatti, Francisco, Ludwig-Müller, Jutta, Alvarez, Maria Elena, Welchen, Elina
Format: Article
Language:English
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Summary:Arabidopsis ( ) OXIDATION RESISTANCE2 (AtOXR2) is a mitochondrial protein belonging to the Oxidation Resistance (OXR) protein family, recently described in plants. We analyzed the impact of AtOXR2 in Arabidopsis defense mechanisms against the hemibiotrophic bacterial pathogen mutant plants are more susceptible to infection by the pathogen and, conversely, plants overexpressing (oeOXR2 plants) show enhanced disease resistance. Resistance in these plants is accompanied by higher expression of WRKY transcription factors, induction of genes involved in salicylic acid (SA) synthesis, accumulation of free SA, and overall activation of the SA signaling pathway. Accordingly, defense phenotypes are dependent on SA synthesis and SA perception pathways, since they are lost in / and ( ) mutant backgrounds. Overexpression of AtOXR2 leads to faster and stronger oxidative burst in response to the bacterial flagellin peptide Moreover, AtOXR2 affects the nuclear localization of the transcriptional coactivator NPR1, a master regulator of SA signaling. oeOXR2 plants have increased levels of total glutathione and a more oxidized cytosolic redox cellular environment under normal growth conditions. Therefore, AtOXR2 contributes to establishing plant protection against infection by acting on the activity of the SA pathway.
ISSN:0032-0889
1532-2548
DOI:10.1104/pp.19.01351