Loading…

Rye-derived powdery mildew resistance gene Pm8 in wheat is suppressed by the Pm3 locus

Genetic suppression of disease resistance is occasionally observed in hexaploid wheat or in its interspecific crosses. The phenotypic effects of genes moved to wheat from relatives with lower ploidy are often smaller than in the original sources, suggesting the presence of modifiers or partial inhib...

Full description

Saved in:
Bibliographic Details
Published in:Theoretical and applied genetics 2011-08, Vol.123 (3), p.359-367
Main Authors: McIntosh, Robert A., Zhang, Peng, Cowger, Christina, Parks, Ryan, Lagudah, Evans S., Hoxha, Sami
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Genetic suppression of disease resistance is occasionally observed in hexaploid wheat or in its interspecific crosses. The phenotypic effects of genes moved to wheat from relatives with lower ploidy are often smaller than in the original sources, suggesting the presence of modifiers or partial inhibitors in wheat, especially dilution effects caused by possible variation at orthologous loci. However, there is little current understanding of the underlying genetics of suppression. The discovery of suppression in some wheat genotypes of the cereal rye chromosome 1RS-derived gene Pm8 for powdery mildew resistance offered an opportunity for analysis. A single gene for suppression was identified at or near the closely linked storage protein genes Gli - A1 and Glu - A3 , which are also closely associated with the Pm3 locus on chromosome 1AS. The Pm3 locus is a complex of expressed alleles and pseudogenes embedded among Glu - A3 repeats. In the current report, we explain why earlier work indicated that the mildew suppressor was closely associated with specific Gli - A1 and Glu - A3 alleles, and predict that suppression of Pm8 involves translated gene products from the Pm3 locus.
ISSN:0040-5752
1432-2242
DOI:10.1007/s00122-011-1589-5