I was looking at my own-root plant of ‘Seafoam’ the other day and was remembering what it was like when I first planted it. It was a nice plant in the pot from the nursery and looked very clean then I put it in the ground and it promptly defoliated with a bad case of the spots… I left it alone and this spring it has taken off throwing multiple canes from ground level and is completely spot-mildew free and about 1m high and wide now covered in flowers (which annoyingly have little pollen >8( ). The leaves are nice and dark with a flush of deep red and everything looks good. I don’t spray things at all and this year is a very bad black pot and mildew year… most things are showing some degree of infection from complete defoliation to the odd spot or two with only a few remaining spot-free. So I began wondering about resistance and the role of stress in resistance and whether plants can build up defenses to pathogens in a similar way to animals can (I know that plants have what could be described as immune responses and I know that lots of people have commented on here that some rose seedlings seem to ‘grow out’ of mildew susceptibility) and exactly what was it I was seeing in ‘Seafoam’ here. I started looking for information about horizontal and vertical resistance and found an article (see link) that helped to explain this in easy terms. It’s really very good I think. A few more questions have since popped into my head… do you think this apparent change in resistance in my ‘Seafoam’ is its horizontal resistance kicking in? Do you think that in times of stress (like transplanting, heat and drought… all of which were factors last year), horizontal resistance can be compromised and take some time to kick back in again at which times resistance comes down to vertical or front-line defenses? Another thing I was wondering is do species roses that show high levels of disease resistance have vertical or horizontal resistance or is their resistance due to this ‘gene-for gene’ vertical relationship mentioned in the article? If horizontal resistance is the ability to ‘match’ an immune response (for want of a better term) to a wider range of strains of a pathogen through multigenic resistance is it worthwhile developing breeders that are the result of ‘collecting’ as many different species as possible before introducing them to modern rose genomes? Do species genes become more specific (i.e. vertical through co-evolution with particular pathogens or strains of pathogens), in response to the strains they have in their native habitat and so experience a breakdown of resistance when put in other areas with different strains, and so would it be better to chose species with a wider range than those with a more restricted range? And lastly (for now ), do you think it is possible to grade a rose’s horizontal resistance using phenotypic features (such as % defoliation) using a standard protocol, to gain more insight into which varieties have the greatest depth of horizontal resistance? It would be good, drawing on everyone’s collective experience and resources here, to get a clearer, formal, idea of a rose variety’s broader resistance. I think we do it informally here all the time, however, it would be interesting to see if any interesting pattens would be evident and whether this translates into measureable gains in breeding using the same protocol to measure success.
Those are all very good questions and ones people are struggling to answer.
THis past summer at the American Society for Horticultural Science meetings I presented some work I did with colleagues to ascertain the resistance types in roses in the Earth-Kind trial program. In laboratory settings we innoculated detached leaves of these roses in humid chambers with three different, characterized races of black spot collected in Eastern North America. After about 2 weeks we terminated the experiments rating + or - reactions to rose / race combination and for those with lesions we measured the diameters of such lesions. The diameters are a good indication of relative degree of horizontal resistance- those with smaller lesions are have greater horizontal resistance.
Xue and Davidson in a late 1990’s paper described how they ascertained different types of data to characterize horizontal resistance and found things like leaf area with symptoms, lesion size, and sporulation capacity were very good things to measure.
Vertical or race specific resistance is often gene for gene, but in some work done by Vance Whitaker it looks like there are some instances where there is race specific variability in degree of horizontal resistance too.
There are great mixes of horizontal and vertical resistance too in roses. For instance, there are races that infect ‘Knock Out’, but once infected, there is strong underlying horizontal resistance.
Those are great questions about species range and variability and how that affects the interaction with the pathogen.
That is a very interesting experience too about ‘Seafoam’. It would be interesting to learn more about the different biochemical pathways that influence horizontal resistance and how stresses can interact with them.
The laboratory techniques with known races of black spot and using multiple repicate chambers I suspect is a really good and controlled way to document and compare horizontal resistance. It isn’t perfect, but it is relatively affordable and something that can relatively easily be done.
Thanks David… so you don’t think field tests would offer any useful information wihtout knowing specific races of black spot… assuming that if a wide enough sampling range was used you would encoutner many different strains? I guess there are too many other variables, like stress, that might invalidate the observations.
Field tests are great, but like you say are hard to control so we can really compare across cultivars and have a really confident assessment. For field tests like in Earth-Kind trials roses are blocked across a site for statistical analysis. Most of us aren’t blocking our roses and taking data in such a sytematic way to account for variability across our gardens. Reputations for some roses as disease prone or resistant have build over time and have been communicated which is very valuable. Ultimately it is field data that is the best as it is what we are looking for, the resistance of a rose in the outdoor environment. These detached leaf assays have been shown to be pretty comparable to whole plant innoculations and are a good tool to predict whole plant outdoor performance.
Having a controlled method with documented races/isolates, it can allow us to gather and communicate data quickly. It can allow us to compare across cultivars all innoculated in replicate at the same time to compare differences more confidently.
The University of Minnesota houses 11 races now (some are from Europe) and this resource is being well preserved and ultilized to better characterize resistance genes in roses and help with the ongoing efforts to develop tools and methods for the development of resistant roses.
I’d guess that these are a mere fraction of the blackspot variants that exist but it’s a significant collection nonetheless. It has more potential utility than just being used for research, too.
Bill Radler developed Knockout by literally throwing as many pathogens at his seedlings as he could lay his hands on. For most of us this would be a hard thing to do but it would be way easier if we could obtain innoculant material from such a collection as the University of Minnesota has. Are there any plans to share the wealth, so to speak?
Unfortunately, there are limitations outside their control that races cannot be released into the environment. They will have to be used in the lab and controlled innoculation settings and prevented from being released to the environment.
There are plans to develop this resource and eventually have a subset of the most informative, diverse races available for people to have their roses screened. We are working on a grant now that will hopefully help make this possible as well as more characterization of resistance genes in roses.
Don, I think I would rather see places like Minnesota set up a commercial venture whereby breeders could send plants for evaluation rather than releasing multiple pathogens into an environment where they may not already be present.
So with the Earth Kind roses… I have been living under a rock or something… is there somewhere to have a look at the results? I’ll google too and try and find it that way as well.
The black spot data from laboratory assays from the ASHS meetings this summer isn’t in print yet. We just had a summary abstract for the conference and here between semesters I’m going to try to work on writing the manuscript with some of the coauthors. We’ll present ploidy level of all the roses, those that are resistant to particular races, and then lesion length with statistics for susceptible reactions to help understand relative horizontal resistance between the roses. For the most part the general trend of horizontal resistance being about as effective to all races held up as would traditionally be expected.
How much I would like to get roses with decorative immaculated Ivy like long standing foliage…
The best I know is laevigata… when happy in full sun up in a tree.
Actually my opinion is that complete desease resistance in all environments is out of reach without genetical manipulations.
Among plant families there are different strategies relative to coevolution with desease. Facing or escaping.
Facing is developing the immunity that allows dense solid and multiclonal stands.
Escaping is growing either in airy places, marginal low density places (i.e. desertic) or quite dispersed among other plants. Often pioneering before tree growth.
Roses IMO fall distinctly in the later category. The only solid stands I know of are either windy seaside or higher in mountains above or beside trees.
These different strategies are well studied and illustrated considering African / south American intertropical forests versus some asiatic ones. The former composed of many allways dispersed specimens of species each not being able to grow grouped when the later are said to be often monospecific.
…Not a reason not to work at better relative desease tolerance…
As Don suggested, 11 races of black spot is a good number to use for testing, but do you know how many races have been identified in the U.S.? Is there any clustering of the races with regards to resistance and susceptibility patterns?
Also, are you considering making testing available to rose developers to get a “reading” on disease resistance of particular new varieties? Wouldn’t testing of new varieties provide great comparison data?
I was also wondering what the disribution of rases of blackspot was too… do different races tend to co-exist in the same area? I see different symptoms on different plants but always put it down to being a variety specific response. I’d be happy to send you all my black spot… for the good of science of course
With favourable conditions that are prevalent i.e. in the wetter southern countries all bs strains appears in a few seasons to two years. At least in my experience. Strains that overcome the partial resistances. Be they the same or similar ones.
Places like these are ideal for looking after the elusive better lasting resistance or tolerance.
About this many/most species are quite desease resistant in original environment and not so in unfavourable places.
I would like to have lab test results of some like rugosa, banksiae or laevigata that often are quite healthy and elsewhere not at all. Suggesting a non race specific resistance. Or an environment promoted liability.
That is why while breeding for desease resistance from the best species I have strong doubts about the hability of many to be expressed in a modern rose genetical environment.
I.e. it is a real possibility that wichuraiana species excellent garden desease resistance is partly lost with larger leaflets alone. Same for sempervirens, banksiae high tolerance.
Or that rugosa and bracteata resistance is from villosity and/or leaf puckering so that resistance is readily lost with smooth bald leaved hybrids.
Pierre, those are great thoughts! I hadn’t thought about the physical characteristics possibly having an impact on overall apparent disease resistance. I’ll bet that you are right!
Is anyone working on manipulating the genes of the blackspot fungus Diplocarpon rosae instead of the blackspot host? Crippling the fungus’ adaptability might be more productive than enhancing the host’s resistance.
Cass, that could open up a can of worms - remember “The Andromeda Strain”.
Working with natural enemies is one thing. (This is what I assume happens in my no spray garden of about 1000 roses after around 5 years of “monoculture” Good guys and bad guys reach an equilibrium.); but artifically trying to change fungi - I am scared of that approach.
The paper below suggests that trichoderma harzianum is a promising control.
Title: Biological control of black spot of rose caused by Dipocarpon rosae .
Authors: Prasad, R. D.; Rangeshwaran, R.; Sunanda, C. R.; Vinita, J.
Authors affiliation: Project Directorate of Biological Control, Post Bag No. 2491, H.A. Farm Post, Bellary Road, Hebbal, Bangalore 560 024, India.
Published in: Annals of Plant Protection Sciences,volumn 10, pages 256-259, (2002).
Abstract: “Fungal biological control agents (Trichoderma harzianum , T. viride and Chaetomium globosum ) were used either alone or in combination with fungicides (chlorothalonil and mancozeb) to manage black spot of rose caused by D. rosae under greenhouse conditions. Black spot incidence in biological control agent and/or fungicide treatments was significantly low (disease ratings from 0.33 to 3.33) compared to the control at all observation dates. After 100 days of spraying, defoliation was lowest with chiorothalonil, Trichoderma harzianum +chlorothalonil, C. globosum +chlorothalonil and T. harzianum +mancozeb treatments. The highest mean vigour index was recorded in T. harzianum treatment. The highest flower production was recorded in C. globosum +chlorothalonil treatment (4.33) followed by T. harzianum alone and T. harzianum +chlorothalonil treatment (4.00).”
Cass wrote: “Crippling the fungus’ adaptability might be more productive than enhancing the host’s resistance.”
Or it might be additive and complementary.
One can imagine an harmless not virulent highly competitive selected BS strain inoculated before the virulent ones occurence. Some kind of vaccination as it was done i.e. inoculating tomatoes with low virulence viruses (TMV) strains in order to hinder the virulent ones forthcoming.
But Henry’s paper is more promising as the control is actually achievable using a common funghus habilities.
Henry, I do share your concern that all scientific research be ethically conducted to avoid unintended consequences; however, with better gene mapping, I hold out hope that highly targeted manipulations will be possible some day.
I would expect blackspot’s inherent adaptability to eventually limit the efficacy of biological controls.
), do you think it is possible to grade a rose’s horizontal resistance using phenotypic features (such as % defoliation) using a standard protocol, to gain more insight into which varieties have the greatest depth of horizontal resistance? It would be good, drawing on everyone’s collective experience and resources here, to get a clearer, formal, idea of a rose variety’s broader resistance. I think we do it informally here all the time, however, it would be interesting to see if any interesting pattens would be evident and whether this translates into measureable gains in breeding using the same protocol to measure success.