Potato virus Y induced changes in the gene expression of potato (Solanum tuberosum L.) Marus ˇa Pompe-Novak a, * , Kristina Gruden a,b ,S ˇ pela Baebler a , Hana Krec ˇic ˇ-Stres a , Maja Kovac ˇ a , Maarten Jongsma c , Maja Ravnikar a a National Institute of Biology, Vec ˇna pot 111, 1000 Ljubljana, Slovenia b Joz ˇef Stefan Institute, Jamova 39, 1000 Ljubljana, Slovenia c Plant Research International, Postbus 16, 6700 AA Wageningen, The Netherlands Accepted 27 February 2006 Abstract The tuber necrotic strain of Potato virus Y (PVY NTN ) causes potato tuber necrotic ringspot disease in sensitive potato cultivars. Gene expression in the disease response of the susceptible potato (Solanum tuberosum L.) cultivar Igor was investigated at different times after infection, using subtractive hybridization, cDNA microarrays and real-time PCR. The most pronounced change in the expression pattern of functionally diverse groups of genes was detected in systemically infected leaves 14 days after inoculation, and in leaves of plants grown from infected tubers. The expression of several stress-related genes during the infection process, including those for heat shock proteins, catalase 1, b-1,3-glucanase, wound inducing gene, and genes involved in photosynthesis, suggests their role in the susceptible potato–PVY NTN interaction. q 2006 Elsevier Ltd. All rights reserved. Keywords: cDNA microarrays; Gene expression; Solanum tuberosum L.; Potyviruses; Potato virus Y NTN ; Real-time PCR; Subtractive hybridization 1. Introduction Plant responses to plant pathogens are complex, involving a range of signaling pathways [1], and show a broad spectrum of physiological and histological changes. Depending on the pathogen type, plants can exhibit resistance or sensitivity. Necrotic lesions, one of the most frequent phenomena in plant– pathogen interactions, may occur in both resistant and sensitive plants. In a resistant plant, the pathogen is restricted to the necrotic lesions, which are part of a hypersensitive reaction [2]. The encounter between a sensitive plant and a pathogen results in disease, despite the formation of necrotic lesions [3]. It has become increasingly apparent that the speed and extent of the plant response determines the outcome of the plant-pathogen interaction [4]. Hosts react to virus infection in complex ways defined by the demands of the virus, host defenses, host stress factors, cellular responses and local and remote tissue responses [5]. Most work in the field of plant–pathogen interactions has been carried out on plant–bacterial and plant– fungal interactions, while plant responses to viruses are less well understood. Potato virus Y (PVY), a member of the Potyviridae family, has long flexuous particles of 730!11 nm. The particles contain a single molecule of linear, positive sense, single- stranded RNA [6]. There are different strains, PVY NTN being the most aggressive. Most potato cultivars are susceptible and develop diverse symptoms after PVY NTN infection. In sensitive potato cultivars, PVY NTN causes potato tuber necrotic ringspot disease (PTNRD), which significantly decreases the quality and quantity of the yield. Because of the importance of potato as a crop and the epidemic spread of PVY NTN in Europe and other continents from the 1980s onwards, many physiological and morphological parameters have been studied in PVY NTN infected plants. The cultivar Igor is one of the most susceptible and sensitive varieties to PVY NTN . Symptoms are visible on all tubers as severe necrotic ringspots, and on green parts of the plants. A few days after infection, necrotic spots (local lesions) appear on inoculated leaves, with wrinkles and mosaic chloroses appearing later on non-inoculated leaves, as the virus spreads. A palm tree appearance (leaf drop) arises in both primary and secondary infections [7]. Changes can also be seen on the cellular level. In the necrotic spots, of cv. Igor, Physiological and Molecular Plant Pathology 67 (2006) 237–247 www.elsevier.com/locate/pmpp 0885-5765/$ - see front matter q 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.pmpp.2006.02.005 Abbreviations: dpi, days after inoculation; hsp, heat shock protein gene; HSP, heat shock protein. * Corresponding author. Tel.: C386 1 4233388; fax: C386 1 2573847. E-mail addresses: marusa.pompe.novak@nib.si (M. Pompe-Novak), hana. krecic@nib.si (H. Krec ˇic ˇ-Stres).