Pyrenophora tritici-repentis(Ptr) is the causative agent of tan spot, one of the yield limiting diseases of wheat, rapidly increasing in wheat growing countries including Kazakhstan. The aim of this study was the identifcation of wheat genotypes with resistance to Ptr race 1 and race 5 and their host­selective effectors (toxins) Ptr ToxA and Ptr ToxB. A common wheat collection of 41 accessions (38 experimental and 3 controls) was characterized using the molecular markersXfcp623andXBE444541, diagnostic for theTsn1andTsc2genes conferring sensitivity to fungal toxins. The coincidence of the markerXBE444541with resistance to race 5 was 92.11 %, and with Ptr ToxB, 97.37 %. Genotyping results using the markerXfcp623confrmed the expected response to Ptr ToxA; the presence/absence of the markerXfcp623completely (100 %) coincided with sensitivity/resistance to race 1 and Ptr ToxA. This demonstrates the reliability of the diagnostic markerXfcp623for identifying wheat genotypes with resistance to the fungus and insensitivity to Ptr ToxA. The study of the reaction of wheat germplasm to the fungal inoculation and toxin infltration showed that out of 38 genotypes analyzed 30 (78 %) exhibited resistance to both race 1 and race 5, and insensitivity to toxins Ptr ToxA and ToxB. Of most signifcant interest are eight wheat genotypes that showed resistance/insensitivity both to the two races and two toxins. The results of phenotyping were reconfrmed by the molecular markers used in this study. Sensitivity to Ptr ToxB is not always correlated with susceptibility to race 5 and is dependent on the host’s genetic background of the wheat genotype, i. e. on a specifc wheat genotype. The results of the study are of interest for increasing the efciency of breeding based on the elimination of the genotypes with the dominant allelesTsn1andTsc2sensitive to the toxins Ptr ToxA and ToxB. The genotypes identifed will be used in wheat breeding for resistance to tan spot.

In three independent experiments in Turkey and Kazakhstan, winter wheat germplasm with variable degrees of resistance to leaf rust was subjected to fungicide protection. The yield loss of genotypes susceptible to leaf rust varied from 30% to 60% depending on the environment and severity of infection. Genotypes completely or moderately resistant to leaf rust also responded positively to fungicide protection, with average yield increases in the range 10–30%. This increase was observed even in one season without leaf rust infection. The main character affected by fungicide was 1000-kernel weight. There was stable expression of the magnitude of yield gain in resistant genotypes in different seasons, confirming genetic variation for this trait. Possible mechanisms of yield gain from fungicide protection in resistant genotypes are related to a positive physiological effect of the chemical used as well as a possible ‘cost of resistance’ to wheat plants. The magnitude of yield gain by resistant germplasm justifies its capture in breeding programs to develop varieties resistant to diseases and with greater benefits from the fungicide protection.

Common bunt is known to cause grain yield and quality losses in wheat due to bunt ball formation and infestation of the grain. The aim of this study is to identify for sources of resistance to common bunt in wheat genotypes using phytopathological and molecular methods. In general, studied 60 Kazakh and foreign wheat genotypes were found 15 samples with the Bt9 , Bt8 and Bt11 genes. Carriers of the Bt10 gene include the five varieties. The four resistance genes, Bt8, Bt10, Bt11, Bt9 , and Bt10 were identified in the Karasai variety. Phytopathological and molecular screening of Kazakh and foreign wheat genotypes selected 18 with genes for resistance to the disease. According to evaluation on an artificial infection 19 varieties showed an immune type of reaction. These varieties will be used in breeding programs as donors to create resistant varieties against the common bunt. Thus, approaches can reduce the level of fungicides use and the most effective method to control the common bunt.

Sweet potato is one of the most economically important crops for addressing global food security and climate change issues, especially under conditions of extensive agriculture, such as those found in developing countries. However, osmotic stress negatively impacts the agronomic and economic productivity of sweet potato cultivation by inducing several morphological, physiological, and biochemical changes. Plants employ many signaling pathways to respond to water stress by modifying their growth patterns, activating antioxidants, accumulating suitable solutes and chaperones, and making stress proteins. These physiological, metabolic, and genetic modifications can be employed as the best indicators for choosing drought-tolerant genotypes. The main objective of sweet potato breeding in many regions of the world, especially those affected by drought, is to obtain varieties that combine drought tolerance with high yields. In this regard, the study of the physiological and biochemical features of certain varieties is important for the implementation of drought resistance measures. Adapted genotypes can be selected and improved for particular growing conditions by using suitable tools and drought tolerance-related selection criteria. By regulating genetics in this way, the creation of drought-resistant varieties may become cost-effective for smallholder farmers. This review focuses on the drought tolerance mechanisms of sweet potato, the effects of drought stress on its productivity, its crop management strategies for drought mitigation, traditional and molecular sweet potato breeding methods for drought tolerance, and the use of biotechnological methods to increase the tolerance of sweet potato to drought.

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