Kartierung und züchterische Nutzung von Resistenzen gegen die Weizenblattdürre (<em>Pyrenophora tritici-repentis</em>)

Authors

  • Uta Engelmann Institute for Resistance Research and Stress Tolerance

DOI:

https://doi.org/10.5073/dissjki.2014.003

Abstract

Tan spot is a foliar disease of bread wheat which occurs worldwide. The disease is caused by the necrotrophic fungus Pyrenophora tritici‐repentis (Died.) Drechs. (anamorph: Drechslera tritici‐repentis (Died.) Shoem.). P. tritici‐repentis (Ptr) induces two distinct symptoms on susceptible wheat cultivars. Currently, at least eight races of Ptr have been described based on their ability to form necrosis and/or chlorosis on a set of differential wheat cultivars. The importance of tan spot increased in the last years due to changes in cultivation practice (reduced tilling, narrow rotation) and yield losses between 3‐50 % are observed. The development and use of resistant wheat cultivars is the most effective, economically and environmentally way to control tan spot. Therefore, the aim of this study was to assign Ptr isolates, collected in Germany and Hungary, to known Ptr races and to study the genetic of resistance to Ptr in different doubled haploid populations and to detect QTL for resistance. Seven out of 10 single‐spore isolates of Ptr were unequivocally assigned to the different Ptr races based on their reactions to the wheat differential set; they were assigned to the Ptr races 1, 3, 6 and 8 with Ptr race 8 being most frequent with four isolates. Four DH populations (Solitär x Türkis, Jenga x Tuareg, Jenga x Toras, Ritmo x K56822) were genotyped with AFLP‐, SSR‐, and DArT‐markers and genetic maps were constructed comprising 941.3 cM to 1404.8 cM. The DH populations were evaluated for Ptr infected leaf area in field tests, greenhouse experiments and detached leaf segment tests. In all experiments significant differences between genotypes were observed and the resistance to Ptr turned out to be inherited quantitatively. Based on the field test data of the populations Solitär x Türkis and Jenga x Tuareg resistance QTL were detected on chromosomes 1A, 3B, 5A and 1A, 2B, 4D, respectively. In both populations a major QTL on chromosome 1A was detected explaining 21.9 % and 27.8 % of the phenotypic variation, respectively. In addition, the populations Solitär x Türkis and Jenga x Tuareg were inoculated with Ptr isolates ASC1 (race 1) and A195 (race 8) at two development stages (BBCH13 and BBCH23) in the greenhouse. In both populations QTL on chromosome 1A were identified which are identical to the major QTL detected in the field experiments. Further QTL were mapped on chromosomes 5A and 5B in the population Jenga x Tuareg. Furthermore, six QTL for resistance against the Ptr races 1 and 8 were detected in the population Solitär x Türkis which explain between 7.2 % and 15.9 % of the phenotypic variation. Based on detached leaf segment tests with Ptr‐isolates A195 (4 populations) and ASC1 (1 population) 13 QTL for resistance to Ptr were detected. They are located on chromosomes 1A, 1D, 2B, 3B, 4A, 5B, 7A and 7B. The results of the detached leaf segment tests should be treated with care as only a moderate agreement with the QTL detected in the greenhouse experiments and the field tests was observed.

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Published

2014-07-01

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Section

Dissertation