Pretreatment of tobacco leaves with low concentrations (5 to 10 mM) of H₂O₂ suppressed hypersensitive-type necrosis associated with resistance to Tobacco mosaic virus (TMV) or Pseudomonas syringae pv. phaseolicola. The same pretreatment resulted in suppression of normosensitive necrosis associated with susceptibility to Botrytis cinerea. This type of H₂O₂-mediated, induced disease symptom resistance correlated with enhanced host antioxidant capacity, i.e., elevated enzymatic activities of catalase (CAT), ascorbate peroxidase (APX), and guaiacol peroxidase (POX) after viral and bacterial infections. Induction of genes that encode the antioxidants superoxide dismutase (SOD), CAT, and APX was also enhanced early after TMV infection. Artificial application of SOD and CAT suppressed necroses caused by viral, bacterial, or fungal pathogens similarly as H₂O₂ pretreatment, implying that H₂O₂-mediated symptom resistance operates through enhancement of plant antioxidant capacity. Pathogen multiplication was not significantly affected in H₂O₂-pretreated plants. Salicylic acid (SA), a central component of plant defense, does not seem to function in this type of H₂O₂-mediated symptom resistance, indicated by unchanged levels of free and bound SA and a lack of early up-regulation of an SA glucosyltransferase gene in TMV-infected H₂O₂-pretreated tobacco. Taken together, H₂O₂-mediated, induced resistance to necrotic symptoms in tobacco seems to depend on enhanced antioxidant capacity.
Nonhost resistance is the most common form of disease resistance exhibited by plants against most pathogenic microorganisms. Type I nonhost resistance is symptomless (i.e. no macroscopically visible cell/tissue death), implying an early halt of pathogen growth. The timing/speed of defences is much more rapid during type I nonhost resistance than during type II nonhost and host ("gene-for-gene") resistance associated with a hypersensitive response (localized necrosis, HR). However, the mechanism(s) underlying symptomless (type I) nonhost resistance is not entirely understood. Here we assessed accumulation dynamics of the reactive oxygen species superoxide (O) during interactions of plants with a range of biotrophic and hemibiotrophic pathogens resulting in susceptibility, symptomless nonhost resistance or host resistance with HR. Our results show that the timing of macroscopically detectable superoxide accumulation (1-4 days after inoculation, DAI) is always associated with the speed of the defense response (symptomless nonhost resistance vs. host resistance with HR) in inoculated leaves. The relatively early (1 DAI) superoxide accumulation during symptomless nonhost resistance of barley to wheat powdery mildew (Blumeria graminis f. sp. tritici) is localized to mesophyll chloroplasts of inoculated leaves and coupled to enhanced NADPH oxidase (EC 1.6.3.1) activity and transient increases in expression of genes regulating superoxide levels and cell death (superoxide dismutase, HvSOD1 and BAX inhibitor-1, HvBI-1). Importantly, the partial suppression of symptomless nonhost resistance of barley to wheat powdery mildew by heat shock (49 °C, 45 s) and antioxidant (SOD and catalase) treatments points to a functional role of superoxide in symptomless (type I) nonhost resistance.
Similarities and differences in the immune systems of plants and animals are discussed in relation to non-specific and specific immunity (resistance), systemic acquired resistance (immune memory), transgenerational immune memory and gene silencing. Furthermore, we attempt to answer the question "what is inhibiting or killing pathogens during the immune (resistance) process"? Therefore, the possible roles of reactive oxygen species and antioxidants in pathogen inhibition are evaluated in different types of plant disease resistance.Keywords: plant and animal immunity, immune memory, reactive oxygen species, antioxidants.If we consider immunity (resistance) to pathogen infections in the case of plants and animals, similarities or analogous mechanisms seem surprising but differences could be also important. The two systems seem to be "so far and yet so close", as was expressed by Maekawa et al. (2011) in an excellent paper. The detailed unraveling of the mechanisms of plant immunity followed vertebrate immunity research with a 40-50 years delay, in spite of the fact that Ward (1902) as early as 110 years ago has shown that some lines of bromes (Bromus inermis) react to infection of a rust fungus (Puccinia dispersa) with an "immune response".The essence of both plant and animal immunity is the recognition and protection against the foreign (the non-self). In the course of immune reactions non-specific and specific plant or animal receptors detect non-specific and specific pathogen elicitor molecules also called antigens in animal systems. The first class of plant or animal receptors recognizes the non-specific "pathogen-associated molecular patterns" (PAMP) or "microbe-associated
Under non-stressed conditions the net photosynthetic rate (P N ) of the mutant plants cbp20 of Arabidopsis was similar to that of the wild type (WT). In response to water deprivation, however, P N started to decrease later in the mutants and remained substantially higher. Thermoluminescence measurements showed that the lipid peroxidation induced by severe water stress was also less pronounced in the mutant than in the WT. Both soil gravimetric and plant water potential data showed that cbp20 mutants lose water more slowly than the WT plants. The drought-induced decline in F v /F m , the quantum efficiency of photosystem 2, and photochemical quenching parameters also started later in the cbp20 mutants than in the WT plants. Thus the restricted gas exchange in the cbp20 mutants does not impair the photosynthetic performance of the plant; however, under drought improved water retention provides significant protection for the photosynthetic apparatus.
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