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References 1. L.A.J. Mur 2007 Hypersensitive response in plants eLS. John Wiley & Sons Ltd
In plants, recognition of a pathogen as an invader may result in the formation of hypersensitive response (HR) lesions, i.e. localized programmed cell and tissue death associated with restriction of the pathogen to the infection site. A transient suppression of antioxidants is known to occur during relatively early stages of the HR. Here we show that the transient suppression of a catalase and an alternative oxidase gene during virusinduced local lesion formation (HR) has similar kinetics in different hosts regardless of the extent of leaf necrotization. Both Nicotiana edwardsonii var. Columbia and a paraquat tolerant N. tabacum biotype display significantly less and smaller necrotic lesions in response to inoculation by two viruses ( Tobacco mosaic virus and Tobacco necrosis virus ) in comparison to control plants ( N. edwardsonii and N. tabacum cv. Samsun, respectively). We found that all of these plant hosts display a transient suppression of catalase and alternative oxidase transcript levels starting within six hours after virus inoculation. Our results suggest that the transient decline in antioxidant activity during early stages of an HR does not significantly influence the extent of localized cell death around infection sites.
One of the most typical and best studied type of plant resistance is the hypersensitive response (HR), a form of localized programmed cell death associated with restriction or even killing of pathogens that often leads to macroscopically visible localized tissue necrosis. It is generally assumed that cell death and resistance within the HR are physiologically and genetically linked. However, there has been considerable speculation about whether cell death is an absolute requirement for resistance conditioned by the HR. This review discusses the relation of cell death and resistance in the HR, in particular, the importance of cell death in this process. We intend to focus on the increasing amount of research evidence showing that in several plant-pathogen interactions, the two main components of the HR-resistance and cell death-can be physiologically, genetically and temporally uncoupled. In other words, HR should be considered as a combination of resistance and cell death responses, where cell death may be dispensable for the plant resistance response. The varying contribution of these two components (i.e. cell death and resistance) generates an array of defense strategies - ranging from extreme resistance to“systemic HR”- applied by resistant host plants in the battle against pathogen infections.
The most important viral pathogens of the cultivated potato are Potato virus X (PVX) and Potato virus Y (PVY), which can reduce potato production up to 80%. Thus resistance breeding is one of the major goals of plant breeders. Wild potato species are good sources of resistance (R) genes. The resistant plants respond to viral infection with hypersensitive reaction (HR) or extreme resistance (ER). HR is accompanied by programmed cell death, while ER localizes the virus at the primary infection site and limits virus replication without visible symptoms. While HR is generally strain-specific, ER can act against a broad spectrum of viral pathogens. This review aims to describe the molecular mechanisms of resistance against PVX and PVY in potato.
Basal resistance (BR, a local resistance against pathogens induced by general elicitors) is a multi-faceted defence mechanism appearing in many shapes and with many given names, such as induced (acquired) resistance (protection, defence), as well as a part of innate immunity. Here, we give a historical overview of concepts, present results and an outlook associated with bacteriological studies in the Plant Protection Institute (PPI). The topics on BR briefly covered are its elicitors, light and temperature dependence, changes in plant physiology, transcription and protein expression during it and its effect on bacteria. We emphasize the importance and relevance of its quick form, early BR, which might be a plant defence mechanism in nature against all kinds of pathogenic and saprophytic bacteria.
Three genotypes of barley (cultivar Ingrid) expressing the genes Mlo (susceptible), Mla12 (resistant with HR symptoms) and mlo5 (resistant without HR) in relation to infection by race A6 of Blumeria graminis f. sp. hordei have been sprayed with a solution of H2O2 after establishment of infection (2-3 days after inoculation). Under the influence of H2O2, leaves of the susceptible Mlo and mlo5-resistant plants exhibited HR-type symptoms with tissue necroses. The Mla12-resistant genotype produced HR earlier and the number of necrotic lesions increased, as compared to untreated control leaves. Treatment with H2O2 before establishment of infection (one day after inoculation), resulted in all the three genotypes in inhibition of the pathogen and symptomless response. It was possible to reverse the inhibitory as well as the HR-producing actions of H2O2 with injection of leaves with a combination of superoxide dismutase (SOD) and catalase (CAT) before treatment with H2O2. It is suggested that the hypothetical negative regulation of HR-associated resistance in susceptible plants carrying the gene Mlo as well as in barley displaying HR-independent resistance and carrying the gene mlo5, could be associated with the limited production of H2O2 in infected plants. Supplying H2O2 to barley leaves that are either susceptible or display HR-independent resistance after establishment of infection, releases the negative regulation of symptoms of HR-associated resistance. This action of H2O2 is sensitive to antioxidant enzymes, such as SOD and CAT.
their activity is the protection of plants against different stressors, such as pathogens [ 14 – 17 ]. Programmed cell death is part of plant defence response typical of an incompatible pathogen–host interaction called hypersensitive response [ 18
It is established that the central area of TMV-induced local lesions developed in detached Datura stramonium leaves, along with the completely collapsed cells (types I and II), contains cells (type III) conserving to a certain degree integrity of their structural components. A characteristic of the type III cells was the accumulation of considerable amount of virus and formation of TMV-specific granular and tubular inclusions. The study of lesion development showed that a proportion of the collapsed cells and cells of type III did not essentially change in the period up from 3 to 5 days after infection of the leaves. These data suggest that the disease development in cells of type III does not lead to a hypersensitive response and is very similar to that in the systemically infected cells.
In spite of the enormous information from research on genetics of plant disease resistance, the question still remains unresolved: what is directly inhibiting or killing pathogens and suppressing symptoms in resistant plants? This is particularly true for resistance to viral infections. Here we show that externally applied reactive oxygen species (ROS) such as hydrogen peroxide (H2O2) or ROS-producing (O 2 ·− [superoxide] and H2O2) chemical systems infiltrated into tobacco leaves 2 hours after inoculation suppress replication of Tobacco mosaic virus (TMV) in the susceptible Samsun (nn) cultivar. This was determined by a biological and a real-time PCR method. Infiltration of leaves of the resistant Xanthi (NN) cultivar with the ROS-producing chemicals and H2O2 significantly suppressed local necrotic lesions (i.e. the hypersensitive response) after inoculation of tobacco leaves with TMV. Accordingly, an early accumulation or external application of ROS, such as O 2 ·− and H2O2, in tobacco may contribute to the development of resistance to TMV infection.
The maize Golden2-like or GLK genes encode proteins belonging to a class of GARP domain transcriptional activators. GLKs have been observed to be involved in chloroplast development and stress adaptation. In spite of the importance of GLKs in plant processes, the in planta targets of GLK regulated transcription, however, have not been identified. We use GLK1 overexpression (OE) to study reprogramming of gene expression networks by GLK1 in Arabidopsis and to identify an associated phenotype. GLK1 OE in Arabidopsis confers resistance to Fusarium graminearum , a broad host pathogen responsible for major losses in cereal crops. Affymetrix Gene Chip and RT-PCR analyses indicated that GLK1 OE in Arabidopsis reprogrammed gene expression networks to enhance a high constitutive expression of genes encoding proteins involved in basal defences but downregulated genes that are associated with programmed cell death and hypersensitive responses. The nature of the role of GLK1 overexpression in selectively reprogramming defence gene networks could explain its effectiveness in enhancing the development of resistance to the necrotrophic phase of F. graminearum pathogenesis.
