Defense activated by 9-lipoxygenase-derived oxylipins requires specific mitochondrial proteins.

Plant Physiol

Centro Nacional de Biotecnología-Consejo Superior de Investigaciones Científicas, Campus Universidad Autónoma, Cantoblanco, E-28049 Madrid, Spain.

Published: February 2013

AI Article Synopsis

  • 9-Lipoxygenases (9-LOXs) are involved in fatty acid oxygenation, leading to the production of oxylipins that help plants defend against certain pathogenic bacteria.
  • A study of Arabidopsis mutants (noxy) revealed that many of them are also insensitive to isoxaben, an herbicide that disrupts cellulose production and cell wall integrity, indicating a link between 9-LOX defense and cell wall modifications.
  • Further investigations identified specific mutations in three noxy mutants that caused mitochondrial dysfunction, suggesting mitochondria are critical for regulating the plant's defense mechanisms and that the response to 9-HOT is influenced by retrograde signaling from mitochondria.

Article Abstract

9-Lipoxygenases (9-LOXs) initiate fatty acid oxygenation, resulting in the formation of oxylipins activating plant defense against hemibiotrophic pathogenic bacteria. Previous studies using nonresponding to oxylipins (noxy), a series of Arabidopsis (Arabidopsis thaliana) mutants insensitive to the 9-LOX product 9-hydroxy-10,12,15-octadecatrienoic acid (9-HOT), have demonstrated the importance of cell wall modifications as a component of 9-LOX-induced defense. Here, we show that a majority (71%) of 41 studied noxy mutants have an added insensitivity to isoxaben, an herbicide inhibiting cellulose synthesis and altering the cell wall. The specific mutants noxy2, noxy15, and noxy38, insensitive to both 9-HOT and isoxaben, displayed enhanced susceptibility to Pseudomonas syringae DC3000 as well as reduced activation of salicylic acid-responding genes. Map-based cloning identified the mutation in noxy2 as At5g11630 encoding an uncharacterized mitochondrial protein, designated NOXY2. Moreover, noxy15 and noxy38 were mapped at the DYNAMIN RELATED PROTEIN3A and FRIENDLY MITOCHONDRIA loci, respectively. Fluorescence microscopy and molecular analyses revealed that the three noxy mutants characterized exhibit mitochondrial dysfunction and that 9-HOT added to wild-type Arabidopsis causes mitochondrial aggregation and loss of mitochondrial membrane potential. The results suggest that the defensive responses and cell wall modifications caused by 9-HOT are under mitochondrial retrograde control and that mitochondria play a fundamental role in innate immunity signaling.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561008PMC
http://dx.doi.org/10.1104/pp.112.207514DOI Listing

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