Loading...
Please wait, while we are loading the content...
Similar Documents
Update on Reactive Nitrogen and Oxygen Species Cross Talk between Reactive Nitrogen and Oxygen Species during the Hypersensitive Disease Resistance Response 1
| Content Provider | Semantic Scholar |
|---|---|
| Author | Zaninotto, Federica Camera, Sylvain La Polverari, Annalisa Delledonne, Massimo |
| Copyright Year | 2006 |
| Abstract | In recent years, nitric oxide (NO) has been identified as a fundamental molecule that interplays with reactive oxygen species (ROS) in a variety of ways, either as a crucial partner in determining cell fate or in signaling in response to a number of physiological and stress-related conditions. The best characterized relationship between NO with ROS refers to its role in plant defense against pathogen attack, in particular in the establishment of the hypersensitive reaction (HR; Wendehenne et al., 2004; Delledonne, 2005). HR is a form of programmed cell death that contributes to plant resistance by restricting the invading pathogen at the infection site and shows some regulatory and mechanistic features characteristic of apoptosis in animal cells, like membrane dysfunction, vacuolization of the cytoplasm, chromatin condensation, and endonucleolytic cleavage of DNA (Greenberg and Yao, 2004). Activation of the HR triggers a number of rapid cellular responses, including perturbations of ion fluxes and changes in the pattern of protein phosphorylation (Lamb and Dixon, 1997), which precede the accumulation of ROS and NO. The oxidative and nitrosative bursts are then followed by a signal cascade that mediates transcriptional activation of defense genes and finally the local and systemic expressionof antimicrobial proteins, leading to the establishment of systemic acquired resistance (McDowell and Dangl, 2000). Theoxidativeburst consistsof abiphasicproductionof apoplastic ROS at the site of attempted invasion. Pharmacological, molecular, and genetic studies strongly support the idea that the primary source of ROS is an O2 2 generating membrane-bound NADPH oxidase (Lamb and Dixon, 1997). ROS have several direct and indirect roles in plant defense: they are directly toxic to invading microorganisms, contribute to the strengthening of cell walls by cross-linking cell wall proteins, regulate the synthesis of new signals such as salicylic acid, lead to enzyme activation and gene expression targeted toward resistance by alteration of redox status, provoke damage to DNA and proteins, and have long been considered crucial in determining cell fate during the HR (Grant and Loake, 2000). Hydrogen peroxide (H2O2) has been shown to trigger cell death following either exogenous administration or genetic augmentation in transgenic plants lowered in H2O2 scavenging capacity (Neill et al., 2002).However, ROS alone trigger a cell death characterized by strong oxidative cell damage that has specificmorphological and biochemical features distinct from those observed in elicitor or pathogeninduced hypersensitivity (Montillet et al., 2005). Starting from the fundamental role in the immune response that NO plays in animals in cooperation with ROS, recent studies have focused on the possible function of NO during the HR (Delledonne et al., 1998). Plants can produce NO through either two main enzymatic systems, namely NO synthase and nitrate reductase, or by several nonenzymatic reactions such as liberation of NO from nitrite under different conditions (Crawford, 2006). During the HR, a peak of NO is produced concomitant with the oxidative burst and with the increase of NO-synthase activity (RomeroPuertas et al., 2004). However, the source(s) of NO during this resistance response has yet to be unequivocally demonstrated. Because of its chemistry and reactivity, NO can have a number of important direct functions in plant defense in parallel with ROS. It can be directly cytotoxic to microbes, affect gene expression by altering the redox status of the cell, regulate protein function through direct posttranslational modifications, and provoke damage to DNA and proteins (Stamler et al., 2001). Moreover, NO can exert important indirect signaling functions through the activation of the cGMP-dependent pathway, which mediates the expression of defense genes such as Phe ammonia lyase and chalcone synthase (Durner et al., 1998). Most importantly, a large body of pharmacological and genetic evidence has demonstrated that NO is essential, together with ROS, for triggering cell death during the HR (Romero-Puertas et al., 2004). |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://profs.sci.univr.it/delledonne/Papers/2006%20Zaninotto%20PP.pdf |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
