Are there any wild rose varieties which greatly increase blackspot resistance in offspring? Which would you say are the best for this?
I don’t know of any native North American roses that get BS. Rosa wichurana, as found in van Fleet (New Dawn), or Silver Moon looks resistant too. If R multiflora gets BS, it is not enough to matter in the wild obviously. These latter two species do get anthracnose which sometimes is mistaken for BS. The challenge is that by the time you do enough back crosses to stabilize repeat blooming, you’ve lost the BS resistance most times. So I see the problem as one of getting the repeat-blooming gene into a native species context, more than moving BS resistance into repeat-blooming roses…
Here is a posting by Henry from 2005 of a study that lists black spot resistance of quite a few species. You have to keep in mind that BS resistance is going to vary from plant to plant even among the species. I have two R.blandas plants that I transplanted to my yard and one definitely has better disease resistance than the other. I keep the other one because it’s thornless. I wouldn’t say the natives are immune to BS but like Larry mentioned about R.wichuriana and R.multiflora, the native are more susceptible to spot anthracnose, so that is prevalent disease you’ll see on them. That and powdery mildew, downy mildew and sometimes rust.
If you did a search of the forum you’ll find many postings about disease resistance of the species.
http://www.rosebreeders.org/forum/viewtopic.php?f=2&t=6426&p=6426&hilit=species+black+spot#p6426
The Rose Manual (1933) p 265-268
J H NicolasRose Infections
Summer defoliation > is not always due to disease, although diseases will precipitate it. Summer defoliation did not bother our fathers before the introduction of Austrian Briar blood. Austrian Briars will lose their foliage early because it matures early. It is the nature of the beast that nothing can change, and all their hybrids inherit that character in a greater or lesser degree. When the foliage is mature, the “cortex” or film of corky material that heals the pores where the leaf is attached to the branch begins to form, the leaf receives less and less nutrition from the plant and drops at the least provocation, spray or dust notwithstanding. Some varieties when plants are healthy will push on new leaves at the top as fast as the bottom ones drop and the plant retains its “activity,” but if the defoliation is premature and accelerated by disease faster than new foliage can be produced the plant goes dormant. Pernetianas are at best in regions of long vegetative season, like southern France, the birthplace of the race, divided in two distinct growing periods—an early spring and a long springlike autumn intervened by a hot summer, because there is enough growing weather when they awake from their summer rest enforced by natural defoliation to come again to a useful life, and the new growth has time to mature before winter, if winter there is. Pernetianas are out of place as autumn bloomers where the season is short between a late spring and an early winter.
Black Spot > starts from the inside, but is induced and spread by outside atmospheric conditions. As proof of this Cochet offers the argument that black spot always attacks the older leaves as they mature. If it did start from outside it would attack the soft new foliage just as mildew does, but the moisture inside young foliage is in rapid motion to and from the roots and has no time to mold even when inoculated until that motion slows down in the process of maturity. Black spot is intimately related to the innate persistence of foliage, as above stated; long-lived foliages, such as pure Teas and species evergreen in their native habitats are immune. As Lambert said, "Have you ever seen black spot on > bracteata, sempervirens, Cherokee?> " When Pernetiana foliage has reached near maturity and the weather is humid, the moisture inside the leaves is not evaporated fast enough nor reabsorbed by the plant, and a fungus or mold forms just as clothes fresh from the aseptic laundry process will mold if put away moist.
Although black spot starts inside, the fungus fruits outside through punctures, and infection spreads rapidly to foliage already in process of maturing, there finding a fertile ground even if weather conditions were then normal for proper evaporation of excess moisture in the leaf tissues. This foliage has to be kept insulated by some medium. They do not like dust over there but prefer copper sprays. Another point brought to me to support that theory is that true Hybrid Teas do not take the spot until very late (if they do at all), when part of their foliage has naturally matured, which process is much later than Austrian Briar hybrids. Where summer weather is normally sultry, stick to the old line Hybrid Tea.
Cankers. > Caused by fungi of various identities (see page 186). Like black spot, the disease starts from the inside. There is much analogy between the mechanical line of march of both diseases, too much moisture in the tissues. Canker is especially active in the autumn when late growth has been stimulated and, full of sap, is checked by frost or cold nights. In the spring it is brought about by late frost after the tissues have become full of sap. The sap is “killed,” the inactive moisture becomes “stale,” and fungi develop from the inside, but bloom outside and infest other plants or soft parts thereof. Where black spot is prevalent there is bound to be canker, and the control measure for one gets the other. In Lambert’s place I noticed some wichuraiana climbers infested with a brown canker (not “brown” canker as defined by Miss Jenkins). I called his attention and he said that they have it in years when a late frost came after vegetation had started.
Karl, I like these historical vignettes but they do tend to confuse novitiates rather than inform them. Can you furnish something more recent that states the actual etiology of Diplocarpon so we aren’t left thinking it gets sucked up by the roots and burst forth from the leaves…
Nicholas was writing around 1930, and was at heart a poet. So he used rather picturesquely descriptive language instead of straight modern science. He didn’t say how the disease proceeded from within, but observed that it arose early in the season when the weather was right. In that he is correct according to the most recent wiki article, various Ag Expt Station bulletins and at least one 21st century German dissertation that I came across this evening. There are various claims made but generally it is assumed that the disease primarily over-winters in stems and dropped leaves. Some places claim that the spores do not survive long on their own. I sort of doubt that but don’t have any evidence one way or the other.
It does seem likely that the earliest infections arise without obvious external source. It certainly is true, and well documented, that long periods of high humidity and suitable temperature are needed for germination of the over-wintered spores. I wouldn’t be so mystical about the vital essences of a rose bush, but maybe I’m just not into feng shui, and prefer chai to chi. Once leaves are infested they shed, prolifically, many spores that can infect other places on the same plant or wherever the wind blows them. I have repeatedly noticed with my sporadic spraying program (hardly a program) there is a huge sudden outburst of spotting when the peak heat of summer gives way in August to somewhat cooler nights with dew forming. Very likely the infections were there for weeks, but their growth to sporulation was held in check by high temperatures. So, Nichlas’ cultural observations are probably correct, even if he’s a bit off on the etiology.
As for the Austrian Brier theory of susceptibility I rather doubt it is so simple as that. However, many moons ago I did some naive experiments with ethylene treatment of rose cuttings. Different CVs vary widely in their susceptibility to leaf drop in response to ethylene. D rosae produces a lot of ethylene, or stimulates the plant to do so, I’m not sure which. One thing I recall at this long remove, R wichurana is much less susceptible to ethylene than Crimson Glory. CG produced callus all over the place, particularly on the cut stem end, and where the leaves were previously attached. So mature leaves, or pernetiana leaves, may drop more easily just because they are ready to be nudged in that direction by ethylene. I find it really surprising that there is only one publication on the connection between blackspot and ethylene. Perhaps the same non-silver inhibitor of leaf drop used in floral preservatives would help against BS damage.
It’s not a native, but you might want to try Darlow’s Enigma. A hybrid musk white. Pure white flowers borne in clusters of 50 to 100. Growth large, 10 x 10 ft. Seedling of unknown parentage. It’s almost thornless and highly resistant to disease. I’ve had three of them. Others are using this now for their crosses. Introduced in 1995 by Heirloom Roses.
Thanks for that, Larry.
We really should build a list of Diplocarpon resistant roses and post it on the member’s pages. If this thread produces enough suggestions I’ll do just that.
I can personally recommend these Barden Atomics: Castle Bravo, Cannikin and Diablo Hawk, all of which are cane and bud hardy here on the western Massachusetts - Connecticut border in zone 5B. Paul’s got a new one out that I don’t yet have, Dakota Redwing, but no doubt it will be a valuable addition to the arsenal.
If you can get your hands on anything that Henry Kuska has distributed they would be likewise valuable. I raised several seedlings from his give-aways that are now foundation breeders for my program.
While not evergreen, native R. virginiana is bullet proof and quite fertile with moderns (being tetraploid). Here’s an F1 hybrid incorporating virginiana’s health, vigor and cane color with Aloha’s polypetally, carotenoids, large petals, vigor and increased stature which is not bad in a single step:
I think this might be of little use, but, I am in the grape industry here in Australia and what we do for any of our diseases is to spray at the end of season and again at the start with a Copper and or Sulphur spray. Any of the spores that can be on the plant prior to dormancy and prior to budburst are attacked with these sprays, some vineyards go to the length to spray under the canopy/dripline so to alleviate if possible any spores that might have reached the ground due to rain or wind.
Thanks for those pics, Don. I love what R. virginiana can do in the first generation when crossed with moderns. It definitely adds hardiness, vigor, and lovely foliage. I have seen in virginiana F1’s obvious variation in blackspot susceptibility, from apparent immunity to some pretty ugly spotting.
I had thought about doing Aloha x Suzanne as a re-do of the Red Dawn x Suzanne cross. It would be fun to then cross [Aloha x Suzanne] with your virginiana hybrid.
I’d like to try Castle Bravo and Cannikin.
About Henry’s roses…I got from Jackie some seedlings of Henry’s [calocarpa x nutkana] x acicularis OP. They are still in 4" pots and haven’t bloomed, but for some reason I’m in love with the things. They just seem so robust and tough. I can’t wait to see how they do in winter, what the blooms are like, what the shrub form will be like.
I did not quote Nicolas as a mere curiosity. His statements were based on the observations of three expert rosarians. As such, they are worth more than a quick glance.
You seem to be hung up on the “germ theory” of blackspot. Were Cochet, Lambert and Nicolas wrong in reporting that blackspot was not a problem with older garden roses, even the early HTs?
Here is a more recent quotation:
Journal of Plant Biology 51(1): 11-19 (January 2008)
Protein degradation and nitrogen remobilization during leaf senescence
Juan Liu, Yun Hai Wu, Jun Jie Yang, Yu Dong Liu, Fa Fu Shen
Leaf senescence, a type of programmed cell death, is a complex and highly regulated process that involves the degradation of macromolecules, including proteins, nucleic acids, and lipids. Nutrients, especially nitrogen, are re-mobilized from senescing leaves to newly developing tissues or reserve organs.
I have another from 2013, but it says much the same thing in more words.
Accepting this description of leaf senescence, the problem with the Pernetianas may come down to two questions: Which? and When?
From what I have gathered of the life habits of Rosa foetida, it has a brief but lively growth period beginning in late Winter and continuing 3 or 4 months. It then sheds its leaves and slips into a very long dormancy.
Tea roses, to the contrary, may continue growing all year without a proper dormancy. Old leaves may eventually outlast their usefulness and be cast off. Or, as in other continuously growing plants, nitrogen deficiency may induce the plants to scavenge the oldest leaf to nourish a new one.
When these radically opposed life habits were combined in the Pernetianas, something had to give. Specifically, the Foetida influence (meaning, the genes and patterns of gene regulation) would push the leaves to senescence, transport the recovered nutrients into storage organs (axial buds? cambium? roots?), and then go dormant in order to avoid the heat of summer. Unlike Foetida, the Tea roses generally thrive on heat. Thus, while the Foetida influencing is nudging a Pernetiana into dormancy, the Tea influence would be pushing the plant into growth, and would be reallocating nutrients from the old leaves into new ones.
Approached from this angle, the defoliation associated with blackspot may be seen as an aspect of Foetida’s summer dormancy that is usually masked in “modern” roses. Which is to say that blackspot, considered as a disease, has its origin inside the plant - in the senescence of the leaves.
Furthermore, I have inferred that Rosa foetida, wherever it really originated, derives all (or most) of its moisture from water stored in the soil (from melted snow) rather than from rainfall during the growing season. Other factors aside, we could not expect it to have any particular resistance to fungi grown from spores that germinate on its leaves following prolonged periods of high humidity. The Japanese R. wichuraiana, on the other hand, reportedly grows on beaches, where it must be exposed frequently to mist and spray. Likewise for R. rugosa.
That sounds very much like what I had theorized years ago, Karl. “Confused” instructions to hurry and use up the foliage then refuse to shed it, leading to old, tired, sick leaves.
While I was writing yesterday, my dog started barking to inform me that someone was coming to the door. I had to submit the post before I was quite done.
Stated simply, it takes two to tango. There can be no disease where the prospective victim refuses to dance. Thus, one cause of the disease is internal to the plant. Secondly, there can be no disease where environmental conditions (e.g., temperature and humidity) do not support the growth of the prospective “etiological agent”. That’s the external cause.
New York State Flower Growers Inc. Bul 142 (Oct 1957)
Will Black-Spot Infect Misted Roses?
Robert O. Miller
Dept. of Floriculture, Cornell University
Leaf temperature may be a decisive factor affecting the number of lesions developing on inoculated plants under mist. Experiments have shown that the amount of infection or spore germination drops off markedly below 55°F. and above 85°F. Reduced leaf temperatures under mist thus may have reduced infection in the winter and increased infection in the summer.
http://hortscans.ces.ncsu.edu/library/floriculture/doc_id/3016/Will-Black-Spot-Infect-Misted-Roses.pdf
I think it is important to distinguish between an opportunistic infection by D. rosae of old leaves that are already half-dead, and a devastating defoliation of a previously healthy plant. A few black spots on the occasional old leaf does not imply that the specimen/cultivar is susceptible to the disease called “black spot”.
Has anyone seen a previously healthy Tea rose, HP, Bourbon, China, Noisette, Polyantha or early (pre-Pernetiana) HT become defoliated by black spot under ordinary cultural conditions? How about the very mixed ‘Gloire de Dijon’?
I spent many happy hours at the SJ Heritage over the years I lived in the area, but black spot was not a problem there because of the soil or climate. So, I wasn’t able to make any useful observations on the subject. Currently I awake most mornings to find my roses with damp leaves due to rain, dew or mist. No spots, yet, but maybe later. Both ‘Snowfire’ and ‘Mirandy’ have some remote Pernetiana heritage, coming down through ‘Crimson Glory’. The rose I purchased as ‘Therese Bugnet’ is not that. It is deep red in the bud, but no open blooms yet so I don’t know what it really is. Other roses I have are not descended from Pernetianas.
BTW, the idea of conflicting “constitutions” being involved with disease is not new with me. For example, “… in a spectacular series of experiments in 1950s, Dr. Janet Harker showed that cockroaches containing two pacemakers entrained several hours out of phase with each other (e.g., NYC time in the left lobe and New Zealand time in the right lobe) developed intestinal cancer—something rarely seen in insects.”
http://circadiana.blogspot.com/2006/01/serotonin-melatonin-immunity-and.html
HortScience [38(1):71-74. 2003]
Changes in Mineral Nutrient Concentrations in Petunia Corollas during Development and Senescence
Sven Verlinden
Division of Plant and Soil Sciences, West Virginia University, Morgantown, WV 26505
Abstract: > To observe changes in the nutritional status of corollas during development and senescence, Petunia xhybrida cv. Mitchell corollas were analyzed for macronutrient and micronutrient content, dry weight, fresh weight, and ethylene production. Carbon content decreased at slightly lower rates than dry weight during corolla development between anthesis and senescence, while fresh weight and ethylene production followed patterns expected of climacteric flowers. Nitrogen, phosphorus, and potassium content declined during development. Both phosphorus and potassium content gradually declined throughout development with overall losses of about 75% and 40%, respectively. Nitrogen content declined 50% during development but losses occurred only during the final stages of senescence. No significant changes were observed in sulfur, calcium, magnesium, and micronutrient content of the corollas during development. Most elements were present in much lower concentrations in corollas than in leaves. The concentrations of calcium, magnesium, and manganese were about 1-, 5- and 15-fold lower in corollas than in leaves, respectively. Results indicate that remobilization of selected macronutrients from corollas occurred before and during senescence. Taken together with the presence of low concentrations of macronutrients, my data support the contention that petunia corollas are nutritionally inexpensive and therefore easily disposable organs.
The leaves of Rosa foetida are built to last 3 or 4 months. I assume that they are then dropped in time to avoid the summer drought. Other species have leaves that are built to last several months or even more than a year. Hybrids between an evergreen (or nearly) species with Foetida would be neither here nor there. They would probably receive a half-measure of nourishment combined with an unwillingness to shed leaves when the nutrients are used up. The result would be an inability to combat fungal infections late in the season.
I once saw a demonstration of this: I had an African Violet blooming in a terrarium on my desk at work. As soon as the petals passed their prime, they were attacked by a fungus. I considered removing the plant to protect it from the assault, but the experimenter in me left it to fend for itself. Which it did. The fungus did not spread onto the leaves or any other part of the plant.
On the other hand, Burbank (1914) reported on the possibility of selecting for disease resistance.
Moreover, these new mildew-proof ramblers manifest, partly perhaps as an evidence of the vitality that makes them immune to disease, a capacity to produce enormous clusters of the most beautiful flowers that approach the keeping qualities of some of the everlastings.
Some of them will last at least a month, on the plant or when cut, showing thus a degree of permanency hitherto quite unheard of among roses.
It might be possible to test seedlings for their probable disease resistance by measuring the nutritional density of their new leaves. I found a report yesterday with some discussion of how this might be accomplished with a refractometer. It would be useful to learn if there is a strong correlation between degrees brix and resistance to BS.
“The result would be an inability to combat fungal infections late in the season.” Not just later in the season. It was common with “Pernetiana” types to flower and defoliate, or flower and all foliage turn to junk. Goldcrest was a rose LeGrice felt might be a winner due to its intense golden yellow coloring, except the foliage fell every time it flowered. Quite a few of Winchell’s roses performed similarly in a friend’s San Diego field. Many of the earlier Pernetianas rusted and black spotted badly early in the season, much before the issues should have been expected and were seen on other types. In those situations in the Newhall garden, it wasn’t due to water stress as I had discovered that and provided ample water.
Limit between saprophytism and predating are often just question of different strains.
Actual black spot strains are probably quite remote from those prevalent at Nicola’s time.
Good point.
Two questions come to mind:
- Is there evidence that the strains are different, and are now attacking species and cultivars that were not previously affected?
- Could the more susceptible Pernetianas have fostered the development of these new strains of BS?
Both questions are answerable by DNA sequencing of the main BS strains. Just a matter of $$. Rapid evolution and selection of pathogens is common. Consider the story of wheat rust which is documented in a number of places. I believe a similar story exists for a barley disease too. Read it way long ago in the biography of some famous barley breeder, can’t say who. Rice has several pathogens that have many different races found in different regions of the world. New ones pop up about as fast as resistance is bred into the rice.
Viruses diverge a lot faster than fungi, but in 100 years we could have easily a couple hundred generations of BS, probably 2x that. Just as we can trace a rose pedigree based on genes, we could follow the BS to see whether all have arisen from one progenitor strain relatively recently, or whether there are some rather ancient parents lending mitochondrial genes to each other in combination with lots of nuclear genes that drift very slowly. Unfortunately we don’t know what are the host/pathogen pairs of genes that lead to susceptibility or resistance…
That new hybrid roses were introduced claiming superior desease resistance and failed is common place in roses history.
Most introducers were not liars.
Virulent funghal deseases are much speedier and effectively host selected as beside many yearly generations the harming phase is haploid. That means immediate full virulence expression. Instantly additive. Speedy evolution.
Industrial pollution is not to credit for past desease immunity and Pernetianas are not to blame as much as the rise of rose endogamy. Earlier roses were diverse and close to species.
Add development of rose culture with HT only rose gardens and simple var large plantings that were favorable to the rise of BS virulence.
That is why more diversity is the answer much more than generalisation of the best resistance genes i.e. through genetical manipulations as so many are working at.
This little bit I am about to add might be totally wrong. First off was it Bill Radler which started out somehow with his crosses to eliminate BS by have his roses fighting BS by building up their own immunity ? Could this be also how Kordes plus some others have reduced BS in their new offerings.
The next part might be to far left field. I have three potted roses in a wheelbarrow, they are awaiting a garden to go in, they are kept alive by rain and tap water. After the last lot of rain they “produced” a nice array of BS. I had this thought to make up a permanent bath for some sort of trial and water, feed, induce new growth, to replace the BS leaves to see if they can become immune or “out grow” BS.
I may not have have explained myself well, but I understand what I mean.