Ulvan-induced resistance in Arabidopsis thaliana against Alternaria brassicicola requires reactive oxygen species derived from NADPH oxidase

2015 ◽  
Vol 90 ◽  
pp. 49-56 ◽  
Author(s):  
Mateus B. de Freitas ◽  
Marciel J. Stadnik
2010 ◽  
Vol 37 (6) ◽  
pp. 532 ◽  
Author(s):  
Tony Remans ◽  
Kelly Opdenakker ◽  
Karen Smeets ◽  
Dennis Mathijsen ◽  
Jaco Vangronsveld ◽  
...  

Reactive oxygen species produced by NADPH oxidase and oxylipins derived from lipoxygenase activity can signal various stress conditions and have been implicated when plants are exposed to heavy metals. Transcriptional profiling of the 10 NADPH oxidase and 6 lipoxygenase genes was performed after exposure of Arabidopsis thaliana wild-type and NADPH oxidase mutants to 5 µM CdSO4 or 2 µM CuSO4 for 24 h. Under these short exposures to environmentally realistic concentrations of Cd or Cu, plants modulate signalling networks that regulate the onset of adaptive responses. Metal-specific NADPH oxidase genes were upregulated by Cd but downregulated by Cu, and metal-specific lipoxygenase gene expression was observed only after Cu exposure. Genes that are responsive to both metals were upregulated and may be responsive to general oxidative stress. For all metal-responsive genes except RBOHD, distinct responses were observed between leaves and roots, which may be due to different stress intensities and signalling mechanisms. Mutation of NADPH oxidase genes had opposing effects on gene expression after Cd or Cu exposure. Upregulation of LOX1 and LOX6 in the roots after exposure to Cd depended on NADPH oxidase gene expression, whereas LOX3 and LOX6 expression was induced more strongly in NADPH oxidase mutants after Cu exposure. Furthermore, NADPH oxidases regulated their own expression level and that of other members of the gene family when exposed to Cd or Cu. The results suggest interplay between reactive oxygen species and oxylipin signalling under Cd or Cu stress, and are useful as a basis for genetic studies to unravel metal-specific signalling mechanisms.


2019 ◽  
Vol 20 (4) ◽  
pp. 485-499 ◽  
Author(s):  
Evelin Kámán‐Tóth ◽  
Tamás Dankó ◽  
Gábor Gullner ◽  
Zoltán Bozsó ◽  
László Palkovics ◽  
...  

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Shan Chen ◽  
Xian-Fang Meng ◽  
Chun Zhang

Proteinuria is an independent risk factor for end-stage renal disease (ESRD) (Shankland, 2006). Recent studies highlighted the mechanisms of podocyte injury and implications for potential treatment strategies in proteinuric kidney diseases (Zhang et al., 2012). Reactive oxygen species (ROS) are cellular signals which are closely associated with the development and progression of glomerular sclerosis. NADPH oxidase is a district enzymatic source of cellular ROS production and prominently expressed in podocytes (Zhang et al., 2010). In the last decade, it has become evident that NADPH oxidase-derived ROS overproduction is a key trigger of podocyte injury, such as renin-angiotensin-aldosterone system activation (Whaley-Connell et al., 2006), epithelial-to-mesenchymal transition (Zhang et al., 2011), and inflammatory priming (Abais et al., 2013). This review focuses on the mechanism of NADPH oxidase-mediated ROS in podocyte injury under different pathophysiological conditions. In addition, we also reviewed the therapeutic perspectives of NADPH oxidase in kidney diseases related to podocyte injury.


Planta ◽  
2014 ◽  
Vol 240 (5) ◽  
pp. 1023-1035 ◽  
Author(s):  
Jiangli Zhang ◽  
Changsheng Chen ◽  
Di Zhang ◽  
Houhua Li ◽  
Pengmin Li ◽  
...  

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