There have been evaluations of roses, both cultivated and wild, for black spot resistance in the field [20], [37], [38] and [39] as well as in the laboratory with a detached leaf assay using specific races of the pathogen [7], [39] and [40]. This has revealed a wide range of resistance with the highest levels of resistance from wild rose species or in cultivated forms which are just a few generations from a cross with a wild species. Although over the last 30 years, breeders have begun to develop new roses with better black spot resistance, there is still much to accomplish as only 7% of the 400 rose cultivars field tested in the USA showed high levels of resistance [17].
The host–pathogen interactions vary from rampant growth and sporulation of the pathogen in the host to minimal growth and sparse sporulation to a hypersensitive response to no fungal penetration [40], [41] and [42]. Follow up genetic studies have revealed both vertical resistance conditioned by dominant resistance genes specific to the pathogenic race [32], [43] and [44] and horizontal (partial) resistance conditioned by multiple genes [36] and [45]. Thus the breeding challenge is to quickly introgress multiple sources of resistance from the wild species into the cultivated germplasm without the negative species traits. The major approach to this is to find markers that would allow the selection for specific resistance genes and against the general genome of the donor rose.