“…P. tritici-repentis produces various HSTs, each of which uniquely leads to progression of disease on wheat cultivars that are sensitive to that particular toxin (reviewed in De Wolf et al, 1998;Ciuffetti and Tuori, 1999;Strelkov and Lamari, 2003). Of the three HSTs thus far characterized from P. tritici-repentis, two-Ptr ToxA (Ballance et al, 1989;Tomas et al, 1990;Tuori et al, 1995;Zhang et al, 1997) and Ptr ToxB (Strelkov et al, 1998)-have been shown to be proteins, whereas Ptr ToxC is a low molecular weight compound (Effertz et al, 2002). For Ptr ToxA (hereafter called ToxA), the first protein HST to be isolated (Ballance et al, 1989;Tomas et al, 1990;Tuori et al, 1995;Zhang et al, 1997), sensitivity is conditioned by the presence of a single host locus, Tsn1, on the 5BL chromosome (Faris et al, 1996;Stock et al, 1996;Gamba et al, 1998;Anderson et al, 1999) and the ToxA gene in the fungus (Ballance et al, 1996;Ciuffetti et al, 1997); disease occurs only when both the genes are present.…”