I’m still new at this hobby, but in my reading about disease resistance I’ve come upon some interesting material about disease resistance.
I’m trying to figure out this whole thing with vertical and horizontal resistance. From what I gather, vertical resistance is based on a single gene where as horizontal resistance is based on multiple genes. That is an extreme over simplification I’m sure, but I have a question about breeding related to this.
How does a breeder select varieties for horizontal or verticle resistance to say blackspot? I would assume that selecting for horizontal would be preferred, but the selction process…I’m stumped.
Jeff
Thanks David:
I’m not sure how I missed that thread.
So, in consideration of ability to select for resistance, I should be glad that just about everything gets a little bit of blackspot when grown here unsprayed.
Because only then (with at least a little disease) can one see the differences in severity.
Here are a few pictures illustrating the typical Fall disease status of a few roses here:
So… unless I can find at least a little disease on ‘Blush Noisette’, and those two other seedlings, it would suggest that they might have a vertical [one-gene] resistance that would hide what level of horizontal resistance they have. And then, they might not be good starting material, in a horizontal resistance breeding campaign???
I wonider if Blush Noisette being so close to two species roses if that wouldn’t suggest something more than verticle resistance? Could the combination of genes from Rosa chinensis and Rosa moschata give it horizontal resistance?
There are no species roses that are unaffected by disease.
What makes it appear that species are superior to hybrids is the fact that, in the wild, they reproduce annually and so generate a steady stream of progeny some of which will be resistant to existing disease strains. Any such offspring will eventually become vulnerable to newly emerged disease strains. For ‘horizontal’ resistance mechanisms this process takes longer than for 'vertical resistance mechanisms but it is inevitable.
In the wild this game of leap-frog is eternal. In the domestic garden we have hybrids whose genes have been frozen in time so that diseases have plenty of opportunity to evolve beyond their ability to resist.
Thus, the secret to breeding for disease resistance is to continually generate new hybrids at a rapid pace.
Samplings of Raoul A. Robinson book:
It is impossible to select for disease resistance if that resistance cannot be seen. And it is impossible to measure disease resistance if the disease is absent.
Many parasites also have competitors, which are harmless on our crops, but which also help to keep the parasite numbers down. There may also be antagonistic micro-organisms which restrict the parasite population growth.
(This biologic control complements horizontal resistance)
It is doubtful if even artificially high levels of horizontal resistance will ever provide an absolute control of a crop parasite, in the sense that the parasite disappears completely. But this is a good thing. If we are to maintain a population of hyper-parasites and predators for the purposes of biological control, we must also maintain a small population of crop parasites for them to feed on. This small population will exist because even the maximum levels of horizontal resistance will always permit the parasite to cause minor blemishes that are economically unimportant, but ecologically crucial.
These minor blemishes will maintain both horizontal resistance, the crop parasites, and the agents of their biological control.
Good posts.
Out of the first forty roses worked with for three years only three so far are worthwhile. Now begins the next forty roses. It’s easy to see which seedlings have good horizontal resistance as a group; the patch of green ones surrounded by junk. In second place would be a few good seedlings out of many hundereds as a group. Third place is the group that gets mainly PM and some of everything else without much set back in growth and out of hundereds some with leathery leaves and clean. Neil
Don, I mainly agree with you about the role of competitive evolution in development of better resistant plants. But I think we live in a new age with out instant communications world-wide. So sometimes the onslaught of new diseases comes faster than the mutation/selection process can cope with.
Specifically I think of chestnut blight, Dutch elm disease, and now butternut canker and 1000 cankers disease of walnut. The wooly adelgid attack on hemlock, emerald ash borer and Asian long-horned beetle may be special cases connected to insect dispersals, not fungi per se. However, all reflect rapid communication and transportation of infectious agents across time zones. Blackspot and mildew certainly do travel in commercial materials, far faster than they ever could by breezes alone.
It was claimed by a credible observer (J.H. Nicholas) that Pernet-Ducher lived in a “B.S.-free” zone and was surprised when his Soliel d’Or and others were so vulnerable to the disorder in other locations. We now put incredible, perhaps impossible, demands on our crops for pathogen resistance. Pierre’s quotes immediately above make that point- we must tolerate low level disease to maintain selection against high level infestation. That’s a hard trade-off for the average exhibitor to accept. but it’s absolutely true in the long term.
When it comes to black spot, do the different fungi mutate at all like certain viruses may and are there new races of BS that show up over time?
Rob
The quote “It is impossible to select for disease resistance if that resistance cannot be seen. And it is impossible to measure disease resistance if the disease is absent.” used to be true, but modern genetics is completely changing how this whole process works. In an ever increasingly number of crops, breeders are able to use genetic markers to look directly at the genotype rather than relying on the visible phenotype of disease incidence. This allows breeder to combine multiple disease resistance genes into a single individual, which produces much more robust resistance. As Don pointed out, in the wild or in pure phenotypic selection you get an arms race with the plants evolving resistance genes that are then overcome by new virulence genes on the part of the pathogen. But if you can introduce several resistance genes at once, it becomes much harder for the pathogen to evolve around them because it requires mutations to overcome all of the genes at once.
sometimes the onslaught of new diseases comes faster than the mutation/selection process can cope with.
So then, Larry, does this mean that we are left to be spectators to a great extinction? Perhaps genetic engineering may stave off the Armageddon but:
if you can introduce several resistance genes at once, it becomes much harder for the pathogen to evolve around them because it requires mutations to overcome all of the genes at once.
Joe, this argument replays a controversy over horizontal vs. vertical resistance and gets at the heart of the philosophical divide.
One camp says you are correct, and a lot of money has been spent identifying specific genes for resistance to specific pathogens for that purpose.
The other camp says that this strategy just gets you deeper into the quagmire because you can never stay ahead of the pathogens and a breakthrough mutation risks wholesale extermination of the crop you are trying to protect. They, too, want isolates but for the purpose of screening out plants with race-specific resistance so as to expose those that have horizontal resistance.
It might be worth having a look at Raoul Robinson’s book, see the link below and thanks to Pierre for reminding me about it.
This discussion really confirms, for me, the wisdom of Dennison Morey when he first proposed organizing amateur rose breeders into what eventually became the Rose Hybridizers Association.
Don’t under-estimate the importance of your own efforts no matter how humble they may seem.
http://www.bulbnrose.org/Roses/breeding/Fisher_Morey.html
Link: www.sharebooks.ca/system/files/Return-to-Resistance.pdf?phpMyAdmin=%2Ci00rPh2YR8Tv2gwH2Euk6h7dZ2
Genetic markers are linked to vertical resistance genes. Yes adding as many vertical resitance genes as possible is for many breeders actual answer to vertical resistance genes failures. If one fails, two will stand longer and more even better. The hope is avoiding the first mutation to be crop selected when two or more mutations are needed.
From documented examples Raoul Robinson evidences the spectacular failure of this strategy at specific places where parasites instantly overcome it. Not from instant mutations but just through at random sexual recombination. Potato Blight in Mexico, Corn Rust in tropical Africa…etc… And when a new parasite strain overcomes resistances of a widely grown var ( it is worse for clones) it is only a matter of time it will spread.
And RR emphasise the successes (eventually by farmers alone) with horizontal resistance selection/breeding at these very places as well as historicaly everywhere.
Don, I’d say we are participants, not mere spectators. Maybe not you and I personally, but we as a society. Emerald Ash borer appeared around Detroit but very quickly moved down the turnpike to PA. First appearance there (Cranberry Twp) was right near my mother’s house. Now a couple years later the entire state of PA is in quarantine. And the death front is moving many miles per year.
The 1000 cankers disease of black walnut, which I never heard of until Monday popped up in CA a few years back, perhaps a decade. Spread to NM,CO and in between. Was reported to be in TN. Last summer it was found in Bucks Co., PA which is now under quarantine. But do average people in PA know this- I doubt it. There is a page on a website from some agency but that’s about it. It (the fungus) spreads with a little beetle carried in firewood or air-dried lumber bark. Like Dutch elm disease.
We can expect a blight for every isolated population to come from somewhere and pretty much wipe out whatever evolved in its absence.
On the other hand, the good news. Xanthomonas campestris causes a bad blight in rice and is a curse in Asia. There was dreadful fear when it was being studied here in KS that it might spread to our U.S. rice growing areas. But guess what- it was there already. Climate made it only a minor problem. Maybe B.S. is more like that than chestnut blight.
I think the difference is that the bad blights often require a vector, or have only a limited spread by natural convection. Aphids and rusts migrate seasonally in N.A., so the density of trouble is low enough in the north that they may be selection agents, but not absolute killers.
Remember how early blight of tomatoes wiped out the northeast crop because it was trucked in from seedling growers. It is always present down south but at low levels. It needs perfect conditions, and a high inoculum to become a plague. Of course also it needs the sensitive genotype which was selected in its absence, by use of fungicides.
Robinson makes a lot of good points that may deflate the egos of some plant breeders, exhibitors and perfectionists.
Larry, you make some interesting points. It feels like the list of casualties is growing daily.
For instance, I grow Harry Lauder’s Walking Stick, the contorted hazelnut, a very pretty plant in all seasons. It turns out that this and many other hazelnuts are falling victim to eastern corylus blight and I can expect mine to survive only a couple of more years.
It’s not just plants, either. White nosed fungus continues to ravage bats. The situation for amphibians looks even more dreadful. It may signal a frightening possibility for other species that wholesale extinction is indeed possible.
There is an article about Amphibian chytridiomycosis in this month’s Sigma Xi which you can find here:
Link: www.americanscientist.org/issues/pub/lessons-of-the-lost
What is in the soil probably also contributes to the plants ability to defend itself. I have recommended disease resistant roses to “rose showers”, who attempt to grow roses in soil that resembles a chemical dump, only to have them report that the roses were disease prone.
“Additions of sodium silicate to nutrient solutions affects disease resistance of plants (Belanger et al., 1995) and may enhance the leaf retention of cuttings by inhibiting fungal infection and development. In most research, silicon compounds are applied to plants by adding them to the nutrient solution contacting the root zone (Belanger et al., 1995). Other researchers have found that foliar application of silicon compounds may be superior to root zone application for disease control (Bowen et al., 1992; Menzies et al., 1992).”
http://www.dyna-gro.com/Website%20pdf%20Files/Roses%20-%20Silicon%20Report.pdf
Also see very recent research on the complex behavior of silican on grasses reported below.
Link: www.physorg.com/news/2011-10-defences-mystery-deepens.html