The obligate biotrophic, soil-borne fungus causes wart disease of potato (induces hypertrophic cell divisions in plant host tissues leading to the formation of tumor-like structures. 2, 6 and 18 was correlated and impartial from resistance to pathotype 1. DNA pools were constructed from the most resistant and most susceptible individuals and screened with genome wide simple sequence repeat (SSR), inverted simple sequence region (ISSR) and randomly amplified polymorphic DNA (RAPD) markers. Bulked segregant analysis recognized three SSR markers that were linked to wart resistance loci (on chromosome XI conferred partial resistance to pathotype 1, on chromosome IX to pathotype 18 and on chromosome I to pathotypes 2,6 and 18. Additional genotyping with 191 single nucleotide polymorphism (SNP) markers confirmed the localization of the loci. Thirty-three SNP markers linked to the loci permitted the dissection of alleles that increased or decreased resistance to wart. The alleles were inherited from both the resistant and susceptible parents. Electronic supplementary material The online version of this article (doi:10.1007/s00122-011-1666-9) contains supplementary material, which is available to authorized users. Launch Potato wart is an illness that is learning to be a issue for potato creation in European countries increasingly. The causal agent of the condition may be the obligate biotrophic, soil-borne fungi (Schilberszky) Percival, buy 439288-66-1 which infects tubers, stolons and stems and will cause produce loss up to 50C100% (Baayen et al. 2006; Melnik 1998).The normal disease symptom may be the formation of wart, a cauliflower-like multicellular tissue varying in proportions from few millimetres to many centimetres which has the growing fungus and its own sporangia. Wart tissues includes hypertrophic, tumor-like dividing cells, which surround many, thin-walled summertime and thick-walled wintertime spores or sporangia (sori). The sori have the ability to survive in the garden soil for four years (Laidlaw 1985). The spreading of sporangia occurs through infected tubers or contaminated agronomic tools mainly. Under advantageous climatic circumstances, the sporangia sporulate and infect meristematic tissue through the entire buy 439288-66-1 vegetative amount of potato plant life (Stachewicz and Enzian 1998a, b). As a result, the pathogen represents a long-term garden soil contamination issue, especially in areas with moderate temperature ranges (8C10C) and high garden soil dampness (50C80%). In European countries, the Turkey and Ukraine, 38 pathotypes of have already been identified up to now (Baayen et al. 2006; ?ak?r et al. 2009). Pathotype 1 is well known since very long time and is recognized as the normal pathotype. Recently, new pathotypes had been buy 439288-66-1 found that overcome the level of resistance to pathotype 1. On the other hand, pathotypes 2, 6 and 18 as well as pathotype 1 represent one of the most broadly distributed and intense types of the fungi (Stachewicz 2002). Chemical substance control of isn’t possible. The just ways of confine the condition are tight quarantine and phytosanitary procedures on the main one hand, as well as the cultivation of resistant cultivars CD164 in the various other. Infected plant life need to be demolished and areas infested with aren’t allowed to end up being planted with potatoes buy 439288-66-1 for at least 20?years. Security zones are only allowed to be planted with cultivars resistant to the detected pathotype. Besides reduction of crop yield and quality, the main economic losses result from the phytosanitary steps, which prevent further potato cultivation on infested fields. Before World War II, wart was one of the most important potato diseases. The buy 439288-66-1 introduction of quarantine steps and of varieties resistant to pathotype 1 were successful in controlling the disease. However, only 4% of the current German varieties are resistant to all four pathotypes 1, 2, 6 and 18, and.