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In search of the relationship between the rye polyamine oxidase (PAO) gene and resistance to powdery mildew (PM)

Powdery mildew (PM), a common cereal disease in cultivated areas, including Europe and other temperate regions, is caused by the fungus Blumeria graminis. While PM is one of the most important wheat leaf diseases globally, rye is highly tolerant to PM. It has been reported that in barley infected wi...

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Detalles Bibliográficos
Autores principales: Milczarski, Paweł, Góralska, Magdalena, Pałatyńska, Kinga, Wysoczański, Bartłomiej, Czyczyło-Mysza, Ilona, Maghuly, Fatemeh, Myśków, Beata
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Berlin Heidelberg 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9836972/
https://www.ncbi.nlm.nih.gov/pubmed/36178587
http://dx.doi.org/10.1007/s13353-022-00723-x
Descripción
Sumario:Powdery mildew (PM), a common cereal disease in cultivated areas, including Europe and other temperate regions, is caused by the fungus Blumeria graminis. While PM is one of the most important wheat leaf diseases globally, rye is highly tolerant to PM. It has been reported that in barley infected with PM, polyamine oxidase (PAO) activity related to the production of hydrogen peroxide (H(2)O(2)) has increased, which may promote defense against biotrophic or hemibiotrophic pathogens. The current study aimed to assess the relationship between the segregation of the polymorphic marker for rye PAO (ScPAO) and the level of PM infection in plants. The genetic mapping in two interline populations shows that ScPAO is located on chromosome 7R. Further analysis comparing ScPAO location to mapped wheat (Triticum aestivum L.) PAO duplicates suggests the ScPAO homology with TaPAO6 or TaPAO7. A possible association of ScPAO from 7R with PM resistance is demonstrated in the recombinant inbred lines (RIL)-L population phenotyped for PM infection. Finally, three novel QTLs for PM resistance on the 7R chromosome of rye are detected. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s13353-022-00723-x.