Powdery mildew (PM) of wheat caused by Blumeria graminis f. sp. tritici is among the most important wheat diseases, causing significant yield and quality losses in many countries worldwide. Considerable progress has been made in resistance breeding to mitigate powdery mildew. Genetic host resistance employs either race-specific (qualitative) resistance, race-non-specific (quantitative), or a combination of both. Over recent decades, efforts to identify host resistance traits to powdery mildew have led to the discovery of over 240 genes and quantitative trait loci (QTLs) across all 21 wheat chromosomes. Sources of PM resistance in wheat include landraces, synthetic, cultivated, and wild species. The resistance identified in various genetic resources is transferred to the elite genetic background of a well-adapted cultivar with minimum linkage drag using advanced breeding and selection approaches. In this effort, wheat landraces have emerged as an important source of allelic and genetic diversity, which is highly valuable for developing new PM-resistant cultivars. However, most landraces have not been characterized for PM resistance, limiting their use in breeding programs. PM resistance is a polygenic trait; therefore, the degree of such resistance is mostly influenced by environmental conditions. Another challenge in breeding for PM resistance has been the lack of consistent disease pressure in multi-environment trials, which compromises phenotypic selection efficiency. It is therefore imperative to complement conventional breeding technologies with molecular breeding to improve selection efficiency. High-throughput genotyping techniques, based on chip array or sequencing, have increased the capacity to identify the genetic basis of PM resistance. However, developing PM-resistant cultivars is still challenging, and there is a need to harness the potential of new approaches to accelerate breeding progress. The main objective of this review is to describe the status of breeding for powdery mildew resistance, as well as the latest discoveries that offer novel ways to achieve durable PM resistance. Major topics discussed in the review include the genetic basis of PM resistance in wheat, available genetic resources for race-specific and adult-plant resistance to PM, important gene banks, and conventional and complimentary molecular breeding approaches, with an emphasis on marker-assisted selection (MAS).

Stem rust caused by Puccinia graminis f. sp. tritici (Pgt) is an important disease of bread wheat (Triticum aestivum L.) in South Africa (SA). The frequent emergence of new Pgt races with increased virulence remains a major constraint when genetic control is considered. Monitoring the occurrence, distribution and pathogenicity of Pgt is essential to quickly detect and track new races. During the annual rust survey conducted in 2017, a Pgt isolate (S42-17) collected from wheat in the Free State province near Bethlehem (28.15603oS, 28.28852oE) differed in its virulence profile from known SA Pgt races. Two single-pustule isolates obtained from collection S42-17 were independently phenotyped at the rust laboratories of University of the Free State and ARC-Small Grain, SA. Race analysis was performed using a modified North American (NA) differential set (Jin et al. 2008). In addition to differential lines containing the standard set of Sr genes, Barleta Benvenuto (Sr8b), Coorong triticale (Sr27), Kiewiet triti...

A survey was conducted during 2007 to determine the occurrence and pathogenicity of Puccinia triticina Eriks., the cause of wheat leaf rust, in South Africa. Leaf rust was widely observed in the wheat growing areas of the Western Cape but only at a few localities in the Free State. A low incidence of leaf rust was detected at Cedara (KwaZulu-Natal). Leaf rust widely occurred within trap nurseries but it was observed only occasionally in farmers’ fields. Five pathotypes were identified from the total of 80 leaf rust samples collected. The most frequently detected pathotype was 3SA133 (76.8%) which was found in samples from all the localities followed by pathotype 3SA126 (11.0%). Other pathotypes detected were 3SA140 (7.3%), 3SA132 (3.7%) and 3SA137 (1.2%). None of the isolates tested was virulent on the resistance genes Lr3bg and Lr16 with the majority of the isolates (>73%) found virulent on the resistance genes Lr3a, 3ka, 11, 20, 24 and 30. No isolates avirulent on Lr1, 2c, 10 and 14a were found. The virulence patterns of pathotypes detected in 2007 was similar to those observed in previous seasons and new pathotypes were not observed. Thus, a significant change in the response of current commercial cultivars is not expected considering the results.