**1. Introduction**

Systemic acquired resistance (SAR) is a defence response that initiates immunity to a wide range of pathogens in distant uninfected leaves after a former localised necrotic infection of plants. It was described after tobacco mosaic virus (TMV) infection in tobacco by Ross [1]. In agricultural practice, SAR has been recognised as a strategy to control plant pathogens because of its evolutionary stability [2], long-lasting effectiveness [3] and putative transgenerational effect [4]. Not only pathogen infections but also a number of chemicals and biotic factors

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including hormonal compounds (salicylic acid and methyl jasmonate), benzothiadiazole, Ningnanmycin (an antiviral agent against TMV) and insect eggs have been shown to induce SAR [5-9]. The signal transduction process and its timing are essential components of SAR induction that moves from induced to distant leaves. Recent studies indicated that the movement of SAR signal(s) is connected to plasmodesmata [10].

InductionofSARisoftenvalidatedbytheincreasedexpressionofmarkergenes indistanttissues and/or by limited symptom expression/multiplication of the pathogen. However, the exact evaluation of symptom expression often has serious limitations. Visual assessment ofleaf spots may lead to false analysis [11]. The number of developing TMV lesions is influenced by many factors (especially by the inoculation method and physiological state of plants) and therefore not well suitable as a single factor for characterization of the development of SAR [1,12].

In the present contribution we analysed local TMV lesion size formation and its distribution after SAR induction by a computer-assisted method. The method can detect nearly all lesions on tobacco leaves including the smallest ones (ca. 0.2 mm) and consequently is suitable for the exact determination and comparison of lesion size distribution of differentially treated plants. It is particularly important if a certain component is not normally distributed and mean of data is masking the fine differences. Sherwood [13] rejected normal distribution of fungal lesions (orchardgrass—*Stagonospora arenaria* interaction) in resistant genotypes, but not in susceptible ones. However, to the best of our knowledge, there is no systematic research on lesion size distribution of viral local necrotic infections.

Therefore, our tasks were as follows:

