ARS | Publication request: COMPLEMENTARY GENES FOR CROWN RUST RESISTANCE IN CULTIVATED OAT

Submitted to: Journal of Theoretical and Applied Genetics
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: March 16, 1996
Publication Date: N/A

Interpretive Summary: Crown rust is the most important disease of oat caused by a fungus. The main strategy for control is resistant oat cultivars. To facilitate the development of resistant cultivars, it is important to understand the genetic basis for resistance, and to determine the location of resistance genes relative to molecular markers that can be used as landmarks in breeding programs. Resistance is usually, but not always, controlled by a single gene. We studied an oat population developed from a cross between parents that differed in their resistance to two isolates of the crown rust-causing fungus. We found that resistance involved two separate genes, which were located on different chromosomes. The groups to which these chromosomes belong have been associated with disease resistance in other oat lines and other cereals, suggesting that these chromosomal groups may be important sources for many different types of disease resistance. These results deepen our understanding of the various ways crown rust resistance is controlled in cultivated oat. The results also identify molecular markers that could be useful in breeding programs developing cultivars resistant to these specific isolates of the fungus, as well as indicating areas of the genome that may be rich sources of other resistance genes.

Technical Abstract: Crown rust, caused by Puccinia coronata, is the major fungal disease of oat. Resistance to crown rust is usually, but not always, controlled by single dominant genes in hexaploid oat (Avena sativa). We have examined seventy recombinant inbred lines derived from a cross between A. byzantina cv Kanota and A. sativa cv Ogle that differ in their responses to the two crown rust isolates PC54 and PC59. Analysis of rust infection type data indicates that resistance is not conferred by a single gene in this population. The results indicate that resistance is due to two major unlinked loci which are located on linkage groups 4 and 13 of the molecular map developed from this cross. Additionally, resistance to the two isolates could not be separated genetically, and so both complementary loci appear to be required for resistance to either isolate.