• Korean journal of applied entomology
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• v.12 no.2
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• pp.79-82
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• 1973

1. In order to investigate Physiologic races of Puccinia gramininis f. sp. tritici as basic materials for tile breeding of resistant varieties to stem rust of wheat, this experiment was carried out during 1971 and 1973. 2. Twenty seven isolates of the fungus were identified as follows: two isolates of race 11, eight . isolates of race 17, and 21, four isolates of race 34, one each of race 37 and 56, respectively The remaining three isolates identified were not identical with the key issued by Stakman, et at in 1962. Therefore, the three new races were tentatively numbered $K_3,\;K_4\; and\; K_4,$ in addition to $K_l\;and\;K_2$ described in 1961. 3. Therefore, attempts to produce resistant varieties to stem rust of wheat should be accompanied by intensive investigation of Physiologic races of p. graminis f. sp. tritici in the future.

• The Plant Pathology Journal
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• v.33 no.2
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• pp.125-132
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• 2017

Tan spot (TS), caused by the fungus Pyrenophora tritici-repentis (Died) Drechs, is an important foliar disease of wheat and has become a threat to world wheat production since the 1970s. In this study a globally diverse pre-1940s collection of 247 wheat genotypes was evaluated against Ptr ToxA, P. tritici-repentis race 1, and stem rust to determine if; (i) acquisition of Ptr ToxA by the P. tritici-repentis from Stagonospora nodorum led to increased pathogen virulence or (ii) incorporation of TS susceptibility during development stem rust resistant cultivars led to an increase in TS epidemics globally. Most genotypes were susceptible to stem rust; however, a range of reactions to TS and Ptr ToxA were observed. Four combinations of diseasetoxin reactions were observed among the genotypes; TS susceptible-Ptr ToxA sensitive, TS susceptible-Ptr ToxA insensitive, TS resistant-Ptr ToxA insensitive, and TS resistant-Ptr ToxA toxin sensitive. A weak correlation (r = 0.14 for bread wheat and -0.082 for durum) was observed between stem rust susceptibility and TS resistance. Even though there were no reported epidemics in the pre-1940s, TS sensitive genotypes were widely grown in that period, suggesting that Ptr ToxA may not be an important factor responsible for enhanced prevalence of TS.