Genetic variation and identification of molecular markers associated with partial resistance to Phoma macdonaldii in gamma-irradiation-induced mutants of sunflower

Abstract

A study was undertaken to evaluate the genetic variability among gamma-irradiation-induced sunflower mutants for partial resistance to phoma black stem, caused by Phoma macdonaldii, and to identify putative molecular markers associated with partial resistance. A population of 60 mutant lines and the original line AS613 were evaluated with an aggressive French isolate of P. macdonaldii (MP6) under controlled conditions. Mutants with partial resistance to phoma black stem were identified. Variance in partial resistance and molecular markers, generated with 17 amplified fragment length polymorphism (AFLP) primer combinations, were estimated. Genetic analysis revealed that partial resistance in the mutant line M6-54-1 was controlled by recessive gene(s). The F₁ hybrid (developed by crossing M6-54-1 with a susceptible inbred ENSAT-B4) was, however, significantly less susceptible than the susceptible parent, indicating that the difference between the F₁ hybrid and its parents in reaction to phoma black stem cannot be fully explained by the recessive gene model. Dominance between alleles (epistasis) caused reduced susceptibility in the F₁ progeny, which were also clearly reflected in distributions of phenotypic reactions of F₂ and backcross seedlings. Generation mean analysis confirmed that epistatic effects contributed significantly to genetic variation in phoma black stem resistance in M6-54-1. Using multiple regression analysis, eight AFLP markers associated with partial resistance to phoma black stem were identified. Predicted reactions of all mutants to the disease based on their marker profiles were not significantly different from the observed values. The same AFLP primer combinations were used to map quantitative trait loci in the F₂ population and F₃ families, and one AFLP marker (E33M61-11) was found to be tightly linked to phoma black stem susceptibility.

Keywords:

• AFLP
• disease resistance
• genetic variation
• induced mutants
• Phoma macdonaldii
• sunflower