single dominant gene controls mildew resistance

Title: Isolation and identification of eight races of powdery mildew of roses (Podosphaera pannosa) (Wallr.: Fr.) de Bary and the genetic analysis of the resistance gene Rpp1.

Authors: Linde, M.; Debener, Th.

Authors affiliation: Federal Centre for Breeding Research on Cultivated Plants, Institute for Ornamental Plant Breeding, Ahrensburg, Germany.

Published in: Theoretical and Applied Genetics, volumn 107, pages 256-262, (2003).

Abstract: “Powdery mildew, caused by Podosphaera pannosa, is one of the most-severe diseases of roses grown under glass. The differentiation into physiol. races and the genetic anal. of resistance in a segregating host population was investigated using single conidial isolates of the pathogen. Using ten rose genotypes, all eight isolates of the pathogen could be ascribed to different races. Five races were isolated from one location, which indicates that populations of P. pannosa exhibit a high racial diversity. Infection expts. in a backcross-population of 114 rose plants resulted in a 1:1 segregation, suggesting control by a single dominant gene. Rpp1 is the first resistance gene against rose powdery mildew to be described.”

This is fanatatic to see this work in print and a race-specific mildew resistance gene finally documented. I listened to Debener last summer present a little bit of this work in Toronto. They just happened to find segregation for mildew resistance within the populations they developed and used for characterizing blackspot resistance, double versus single flowers, and thornlessness/thorniness… It’s great that there is so much segregating within these diploid polyantha-like R. multiflora / modern rose descendants they have to be able to do such work. Part of their long term goal is to clone various resistance genes from these populations they are working with and then transform modern cultivars with them. It sounded like they were well on the way with this for the race-specific blackspot resistance gene they isolated and first reported in 1998.




Here follows a completely stupid tought.Yes, something rather idiot:

Do we really believe that a disease-“resistance”-correlated gene, present in a species that had X thousands years to adapt itself to its growing conditions -in a very delimited area- will have the same effect when “extracted” and added to the genetic pool of an hybrid, a totally different one, and grown in a completely different area?

Best wishes,


That’s a great question Pierre. So, even if the “extracted” mildew resistance gene when put in another rose is expressed, it’s true that it’s still just a race-specific resistance gene. It is only effective against a certain virulence allele in the pathogen. We know pathogen populations are variable and often aquire new virulence alleles through mutation or migration of races from other areas. Race-specific resistance is only effective as long as the pathogen doesn’t have the one virulence allele necessary to break down the resistance mechanism of the one host gene. It’s like a time bomb ticking and we don’t know when disease is going to explode.

A more long range goal for practical purposes is to aquire many different race-specific resistance genes (alleles) and stack them in a host. So, by inserting many into one rose the chances are very low that a pathogen can aquire all the virulence alleles to overcome the combo of host race-specific genes. This is a very long term goal as many more resistance genes need to be identified and cloned to do this. So far Debener has reported cloning only one blackspot resistance gene and this recently reported mildew gene.

For practical purposes I believe non-race specific resistance should be emphasized. Debener is the leading molecular geneticist working on roses in the world and no one really comes close to his acomplishments and resources in the rose world now. It’s great that he is focusing on cloning and stacking race-specific resistance alleles, but the rest of us don’t have such tools and cloned genes now. So, by selecting for roses that slow down the pathogen’s life cycle and develop less disease we can make quite a bit of advancement. Non-race specific or sometimes called horizontal resistance typically relies on the action of many genes having relatively small effects. Because of the many genes involved, it’s nearly impossible for the pathogen to accumulate enough mutations to overcome them all. As we select roses that have some disease, but relatively less than others in our seedling populations, we eventually accumulate more and more of these genes having small, but significant effects. It’s harder to select for non-race specific resistance than race-specific resistance where one just looks to find seedlings completely clean of disease (this is so only when the race of the pathogen possessing the appropriate virulence allele to overcome the resistance is not present). To select for such resistance one needs enough disease pressure to see disease, but not too much so as to totally wipe out the seedlings so subtle differences between seedlings can be observed.



Do we really believe that a disease-“resistance”-

correlated gene, present in a species that had X thousands >years to adapt itself to its growing conditions -in a very

delimited area- will have the same effect when “extracted”

and added to the genetic pool of an hybrid, a totally

different one, and grown in a completely different area?

Well, yes and no. 9/10ths of “new” disease resistant apples all have the same resistance gene to Apple Scab.

(In the case of this disease, the “gene” (as I understand it) is actually for hypersensitivity to scab. The fungus attacks and the cells “instantly” die so the disease cannot spread to other cells of the apple.) However, I have heard reports that there is a strain of scab in Europe that can cause scab on these apples. So the fungus will adapt. I don’t know how the powderly mildew gene works in preventing attack.

Last I knew the techniques for inserting genes into other lifeforms was still unperfected. Basically the gene is emplaced scattershot into the cells of a variety, and then testing is done whether the gene took to the cell, and then in each of those cell lines it is tested if it has any actual activity. So getting the gene into a rose variety and having it work may be a fairly difficult task.

So it may work, it may be eventually be overwhelmed by mutations to the fungus, it’s probably going to be very expensive when finally available, and we won’t be allowed to breed from it.

Chris Mauchline