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Genetic mapping of adult-plant resistance genes to powdery mildew in triticale.

ABSTRACT: Triticale is a cereal of high economic importance; however, along with the increase in the area of this cereal, it is more often infected by the fungal pathogen Blumeria graminis, which causes powdery mildew. The rapid development of molecular biology techniques, in particular methods based on molecular markers may be an important tool used in modern plant breeding. Development of genetic maps, location of the QTLs defining the region of the genome associated with resistance and selection of markers linked to particular trait can be used to select resistant genotypes as well as to pyramidize several resistance genes in one variety. In this paper, we present a new, high-density genetic map of triticale doubled haploids (DH) population "Grenado" × "Zorro" composed of DArT, silicoDArT, and SNP markers. Composite interval mapping method was used to detect eight QTL regions associated with the area under disease progress curve (AUDPC) and 15 regions with the average value of powdery mildew infection (avPM) based on observation conducted in 3-year period in three different locations across the Poland. Two regions on rye chromosome 4R, and single loci on 5R and 6R were reported for the first time as regions associated with powdery mildew resistance. Among all QTLs, 14 candidate genes were identified coded cyclin-dependent kinase, serine/threonine-protein kinase-like protein as well as AMEIOTIC 1 homolog DYAD-like protein, DETOXIFICATION 16-like protein, and putative disease resistance protein RGA3. Three of identified candidate genes were found among newly described QTL regions associated with powdery mildew resistance in triticale.

SUBMITTER: Dyda M

PROVIDER: S-EPMC8755695 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:Lesion mimics (LMs) that exhibit spontaneous disease-like lesions in the absence of pathogen attack might confer enhanced plant disease resistance to a wide range of pathogens. The LM mutant, lm3 was derived from a single naturally mutated individual in the F1 population of a 3-1/Jing411 cross, backcrossed six times with 3-1 as the recurrent parent and subsequently self-pollinated twice. The leaves of young seedlings of the lm3 mutant exhibited small, discrete white lesions under natural field conditions. The lesions first appeared at the leaf tips and subsequently expanded throughout the entire leaf blade to the leaf sheath. The lesions were initiated through light intensity and day length. Histochemical staining revealed that lesion formation might reflect programmed cell death (PCD) and abnormal accumulation of reactive oxygen species (ROS). The chlorophyll content in the mutant was significantly lower than that in wildtype, and the ratio of chlorophyll a/b was increased significantly in the mutant compared with wildtype, indicating that lm3 showed impairment of the biosynthesis or degradation of chlorophyll, and that Chlorophyll b was prone to damage during lesion formation. The lm3 mutant exhibited enhanced resistance to wheat powdery mildew fungus (Blumeria graminis f. sp. tritici; Bgt) infection, which was consistent with the increased expression of seven pathogenesis-related (PR) and two wheat chemically induced (WCI) genes involved in the defense-related reaction. Genetic analysis showed that the mutation was controlled through a single partially dominant gene, which was closely linked to Xbarc203 on chromosome 3BL; this gene was delimited to a 40 Mb region between SSR3B450.37 and SSR3B492.6 using a large derived segregating population and the available Chinese Spring chromosome 3B genome sequence. Taken together, our results provide information regarding the identification of a novel wheat LM gene, which will facilitate the additional fine-mapping and cloning of the gene to understand the mechanism underlying LM initiation and disease resistance in common wheat.

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Genetic mapping of adult-plant resistance genes to powdery mildew in triticale.

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