The expression of leaf rust resistance in wheat lines containing Lr12 and Lr13
Bender, Cornelia Magrietha
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Monogenic resistance in wheat (Triticum aestivum L.) to leaf rust, caused by Puccinia recondita Rob. ex. Desm. f. sp. tritici, has generally not been durable. One strategy of attaining durable resistance to rust diseases of wheat is the combination of several resistance genes in a single genotype. Interactions among Lr genes have been defined as the combination of two or more genes resulting in higher resistance levels than that conferred by the genes individually. It has been suggested that Lr12 and Lr13, both adult-plant resistance genes, in combination with other genes, form the basis of durable resistance in several cultivars. In this study, the assumption that Lr12 and Lr13 may interact to condition improved resistance to leaf rust, was investigated. Four Thatcher (Tc) F3 lines (13/12-3, 13112-9, 13/12-19 and 13/12-40), homozygous for both Lr13 and Lr12, were selected and compared with the parents (CT263 [=TcLr13] and RL6011 [=TcLr12]), the single gene lines Tc/13-22 and Tc/12- 16, and Thatcher. In addition to infection type studies in seedlings and adult plants, lines were compared according to several histological and macroscopic components of resistance, as well as disease ratings in the field. Flag leaf infection type studies showed that Lr12 is effective against most pathotypes of P. recondita f. sp. tritici occurring in South Africa. Conversely, Lr13 is ineffective against the dominant pathotypes, implying that the gene has no value as a monogenic source of resistance. Both Lr12 and Lr13 were inherited dominantly. Based on the fact that several pathotypes are avirulent to these genes, they should be manipulated with relative ease in local breeding programmes directed at utilising these sources in combination with other Lr genes. Considering the microscopic components, effects of Lr12 and/or Lr13 resistance on the prepenetration stages were not determined. Results of aborted penetration, consisting of nonpenetrating appressoria and aborted substomatal vesicles, showed that inhibition of fungal growth in wheat lines containing Lr12 and/or Lr13, was activated, to a certain degree, before haustoria were formed. Determination of colony size 240 hours after inoculation indicated that fungal colonies in the combination lines were generally smaller than in the parents, but not necessarily smaller than those in the monogenic line Tc/13-22. Host cell necrosis was more frequently associated with infection sites, specifically of UVPrt2, in the combination lines than in the parents. Hypersensitivity index values (calculated by dividing the area of leaf necrosis with the area of the respective colony), indicated that host cell necrosis was more severe following infection of the combination lines with UVPrt2. Quantification of cell wall appositions showed that fewer papillae occurred in Thatcher than in the other host genotypes. The number of haustoria observed per colony did not indicate any clear, repeatable differences between lines. The common occurrence of host cell necrosis observed during histological examinations was also reflected in the macroscopic components. Infection types on the flag leaves of lines carrying both Lr12 and Lr13 often displayed chlorosis and necrosis. These ratings on primary and flag leaves, as well as the quantitative components including latent period, uredium density and uredium size, did not indicate clear differences between the digenic lines and the most resistant parent. In the absence of a pathotype virulent to both genes, the combination lines were resistant in the field. Field tests with a pathotype virulent to both Lr12 and Lr13 would have been more valid in evaluating whether the genes interacted. Data obtained were not conclusive in suggesting pronounced resistance enhancement due to combining Lr12 with Lr13. Therefore, the assumption of durability, resulting from a novel resistance mechanism conditioned by this combination, was not confirmed.