a b s t r a c tDuring plantevirus interactions, defence responses are linked to the accumulation of reactive oxygen species (ROS). Importantly, ROS play a dual role by (1) eliciting pathogen restriction and often localized death of host plant cells at infection sites and (2) as a diffusible signal that induces antioxidant and pathogenesis-related defence responses in adjacent plant cells. The outcome of these defences largely depends on the speed of host responses including early ROS accumulation at virus infection sites. Rapid host reactions may result in early virus elimination without any oxidative stress (i.e. a symptomless, extreme resistance). A slower host response allows a certain degree of virus replication and movement resulting in oxidative stress and programmed death of affected plant cells before conferring pathogen arrest (hypersensitive response, HR). On the other hand, delayed host attempts to elicit virus resistance result in an imbalance of antioxidative metabolism and massively stressed systemic plant tissues (e.g. systemic chlorotic or necrotic symptoms). The final consequence of these processes is a partial or almost complete loss of control over virus invasion (compatible infections).

Sufficient sulfate supply has been linked to the development of sulfur induced resistance or sulfur enhanced defense (SIR/SED) in plants. In this study we investigated the effects of sulfate (S) supply on the response of genetically resistant tobacco (Nicotiana tabacum cv. Samsun NN) to Tobacco mosaic virus (TMV). Plants grown with sufficient sulfate (+S plants) developed significantly less necrotic lesions during a hypersensitive response (HR) when compared to plants grown without sulfate (−S plants). In +S plants reduced TMV accumulation was evident on the level of viral RNA. Enhanced virus resistance correlated with elevated levels of cysteine and glutathione and early induction of a Tau class glutathione S-transferase and a salicylic acid-binding catalase gene. These data indicate that the elevated antioxidant capacity of +S plants was able to reduce the effects of HR, leading to enhanced virus resistance. Expression of pathogenesis-related genes was also markedly up-regulated in +S plants after TMV-inoculation. On the subcellular level, comparison of TMV-inoculated +S and −S plants revealed that +S plants contained 55–132 % higher glutathione levels in mitochondria, chloroplasts, nuclei, peroxisomes and the cytosol than −S plants. Interestingly, mitochondria were the only organelles where TMV-inoculation resulted in a decrease of glutathione levels when compared to mock-inoculated plants. This was particularly obvious in −S plants, where the development of necrotic lesions was more pronounced. In summary, the overall higher antioxidative capacity and elevated activation of defense genes in +S plants indicate that sufficient sulfate supply enhances a preexisting plant defense reaction resulting in reduced symptom development and virus accumulation.