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Post by DarJones on Nov 2, 2010 8:29:21 GMT -8
This thread is to toss a few thoughts around about horizontal vs vertical disease tolerance. First I'll try to define the meaning of the terms based on literature over the last 50 years.
Vertical resistance - This is generally used to mean use of a single gene to convey tolerance to a disease or pest. The underlying weakness is that single genes can be easy to overcome.
Horizontal resistance - This is used to denote multiple genes which each convey a tiny but useful amount of disease or pest tolerance. A simple way to think of this is that a plant is like a safe with more than one lock. A thief would have to break the combination for the first lock, then the second, third, etc. Obviously, the difficulty of breaking into the safe become greater with more locks.
But as they say, the devil is in the details.
There are well documented examples of single genes that have held up for well over 100 years with no sign of loss of effectiveness. There are other examples of single genes that are effective for only a year or two. Online literature for Maize gives examples of both.
There are examples from potato that show a single gene developing to block a specific variant of a disease. Within a few years, the disease breaks the block, so the potato develops a new gene to block the new variant. One example listed 10 different genes each developed to block a specific disease variant but no single plant contains all 10 genes.
Horizontal resistance is just as muddled. There are plenty of examples such as tomato with fusarium tolerance where some wild tomatoes are essentially immune based on a range of genes that block infection. When those genes are bred into cultivated tomatoes and propagated into millions of plants, the disease breaks the tolerance within a few years. It gets down to a small population of wild plants get less overall disease pressure than a much larger number of cultivated plants.
A very vigorous tomato plant will have some tolerance to nematodes just because the plant can grow new roots to replace infected roots. A less vigorous plant does not express this tolerance. If you combine a vigorous plant with the n1 gene, you get a synergistic effect where the result is greater than either trait by itself.
The relative strength of a gene against infection can also be a major factor. Consider ph2 which blocks some strains of late blight in tomato. Alone, it is no longer effective except on a limited basis. By comparison, ph3 gives a much stronger level of tolerance by blocking to some extent all currently infective strains of the disease.
So what do I take from this? Well, to start with, it is always best to have more than one gene for tolerance to a given disease. When I read of a plant that has (you name the gene) for disease resistance, I am automatically sceptical. I want at least 3 tolerance genes and would prefer 10 or more if they are available.
I'm looking carefully at septoria tolerance because it is the disease that does more damage in my garden than any other. My thought is to identify 5 or more disease tolerant wild plants and try to combine those tolerance genes into a single domestic tomato variety. The presumption is that I would be working with at least 5 and probably more genes for tolerance.
DarJones - just rambling on a Tuesday morning
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joseph
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Post by joseph on Nov 2, 2010 15:25:57 GMT -8
So what do I take from this? Well, to start with, it is always best to have more than one gene for tolerance to a given disease. When I read of a plant that has (you name the gene) for disease resistance, I am automatically sceptical. I want at least 3 tolerance genes and would prefer 10 or more if they are available. My understanding of horizontal resistance, is that it does not depend on finding (or combining) a few individual genes... The horizontal resistance phenomena is due to the combined effects of many, many, many genes... The typical method for developing a crop with horizontal resistance is to eliminate from the gene pool every plant that carries any gene for resistance to the pathogen in question. During the first year of the breeding program any plant that shows resistance is eliminated from the program, and only susceptible plants are continued on to the next year. In this way single gene resistance is eliminated.
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Post by murgatroyd on Nov 2, 2010 18:11:44 GMT -8
My understanding of horizontal resistance, is that it does not depend on finding (or combining) a few individual genes... The horizontal resistance phenomena is due to the combined effects of many, many, many genes... The typical method for developing a crop with horizontal resistance is to eliminate from the gene pool every plant that carries any gene for resistance to the pathogen in question. During the first year of the breeding program any plant that shows resistance is eliminated from the program, and only susceptible plants are continued on to the next year. In this way single gene resistance is eliminated. To clarify for any new members who may be lurking and not familiar with this method, the weeding out of vertical (single gene) resistance carriers early on would be removing plants that show tiny black flecks on the leaves caused by hypersensitivity to the disease organism. Hypersensitivity sacrifices the immediate area around the infection so the disease organism has no living tissue to feed on. After weeding out plants exhibiting hypersensitivity, in some cases it is permissible to even introduce higher levels of the disease organism to speed up the selection process, ultimately harvesting seed from any survivors. This process is called mass selection. Breeding the survivors over and over increases the chance of bringing as many of these beneficial groups of genes together in their seedling descendants as reasonably possible. The book Return To Resistance described mass selection and the difference between vertical (single gene) and horizontal (polygene) resistances very nicely I thought.
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Post by PatrickW on Nov 3, 2010 8:40:46 GMT -8
In my opinion, what everyone is describing here is more vertical resistance than anything else, which can and often does involve more than one gene. This is often achieved with a mass cross and selection.
Horizontal resistance is normally when you have identified a number of separate distinct genes involved in a desired trait, for example blight resistance. You then make deliberate crosses and selections which insure all these separate previously identified genes end up in the same plant at the same time.
This is sometimes called gene stacking, and is often a justification given for why genetic engineering is so useful. After all, the process of using a gene gun to insert the specific genes into one plant is a lot faster than crossing and selection, and in theory should achieve the same result. I'm just saying this to offer their argument, not to justify it myself.
The counter argument would probably be that by doing a mass cross you can also take advantage of unidentified genes or gene combinations that may be present. I'm sure there are many other arguments as well, and probably also others here better able to make the argument.
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Post by murgatroyd on Nov 3, 2010 10:27:03 GMT -8
The terms 'vertical' and 'horizontal' are arbitrary terms. The words red & blue or the letters A & B could just as easily have been used. 'Vertical' shouldn't imply stacked genes.
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Post by murgatroyd on Nov 3, 2010 10:34:30 GMT -8
The counter argument would probably be that by doing a mass cross you can also take advantage of unidentified genes or gene combinations that may be present. If by 'mass cross' you mean crossing the survivors or crossing plants that show less disease pressure, that would agree with what little I know about the mass selection process.
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Post by spacecase0 on Nov 3, 2010 12:17:39 GMT -8
I thought that vertical trusted only one set of genes to protect things, and that it is called vertical because when it falls, it falls totally, just like any vertical object falling. and that horizontal resistance was where you have enough variation so that no new pest could kill all of what you have.
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Post by DarJones on Nov 3, 2010 13:18:21 GMT -8
I think that each of the ideas presented here are valid under at least some conditions. Consider the Chestnut tree. The number of individuals is large but limited and certainly not comparable to the number of stalks of Maize. 100 years ago, the American Chestnut occupied much of Eastern North America. Today, it is down to a few trees surviving as understory remnants that grow back from the roots of trees that were long ago killed by Chestnut Blight. While we can argue all day long that the remaining trees should have developed resistance to the blight by now, useful genes for resistance have not been found. There have been a few scattered trees located that have a very small amount of tolerance but eventually all of them are killed. The Chinese Chestnut happens to have high levels of tolerance to Chestnut Blight. If you read about the American Chestnut Foundation, you will find that a backcross breeding program is nearly at the point of introgressing the tolerance genes into an American Chestnut genetic background. Why is this important for this thread? Because this example shows that you cannot develop polygene resistance unless the genes exist to start with. It also shows that you might go to another species and find the tolerance genes needed. By comparison, Maize is represented by hundreds of billions of plants grown worldwide and therefore a level of genetic diversity beyond anything a tree species can achieve. The point being that developing polygene resistance is much more feasible if you have a large number of plants and a lot of genetic variation to work with. There is online documentation about developing rust resistant maize in Africa. Here is an excellent article about the two forms of resistance which are described as Quantitative and Qualitative. www.ars.usda.gov/SP2UserFiles/ad_hoc/66452500Publications/Balint-Kurti/Balint-KurtiJohalMaizeDisResist08.pdfAs mentioned above, a hypersensitive response where a portion of tissue dies effectively isolating the pathogen is very common. Black Walnut expresses a hypersensitive response to Cherry Leaf Roll Virus. De-toxifying a pathogen's infective chemicals is a second strategy. The HM1 gene in corn specifically produces an enzyme that binds to and breaks down a specific section of the toxin produced by C. Carbonum. Note that it does not permanently bind to the toxin, it just makes it incapable of penetrating the cell membrane. This is an active mechanism where the plant has to produce the deactivation enzyme. Binding to a toxin or directly to a viroid is another strategy to deal with infection. This involves producing a protein that has specific binding points capable of attaching to the infecting toxin or viroid. This is an active mechanism where the plant has to produce the binding protein. Outgrowing an infection is a valid response if the plant can grow faster than the infection can spread. This is a multi gene related plant response that is triggered by infection. A common example of this is a tree responding to fungal infection of leaves by producing a much larger leaf canopy. Producing surface coatings is another tolerance mechanism that some plants use. For example, some plants produce a wax like material on the surface of leaves. This tends to prevent infection by mechanically blocking pathogens. Allelopathy is another tolerance mechanism where a plant produces chemicals that are poisonous to other plants and organisms. Juglone in walnut is an example of an allelopathic chemical in a plant. DarJones
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joseph
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Post by joseph on Nov 4, 2010 16:31:31 GMT -8
So it's been like what? 5 Chestnut tree generations since the blight eradicated most of the American Chestnut trees? It took more than 5 generations for potatoes to recover from their blight, and for African maize to recover from it's blight.
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Post by DarJones on Nov 4, 2010 18:50:09 GMT -8
I think you might be making an assumption that the genes for tolerance exist in the American Chestnut. The best information to date is that it does not. By comparison, the Chinese Chestnut has been exposed to Chestnut Blight for millenia and has a well developed tolerance based on at least 3 significant genes with minor effects from some others.
You might ask why would we care about resurrecting the American Chestnut? The answer is simple. The American Chestnut was a timber type tree that produced tall straight trunks of very rot resistant wood. Chestnut was used to build houses, furniture, rail fences, as crossties, and innumerable other uses. By comparison, the Chinese Chestnut is an umbrella type tree that is not adapted to growing in a forest environment and does not produce comparable wood.
I keep finding that I have the wrong expectations about what can and can't be done with the genetics available. The best example I can think of is the tomato which has an extremely restricted genetic base. No matter how much you might want to, you can't breed a highly disease tolerant tomato based on the domestic variety. The genes just don't exist in Solanum Lycopersicum. But you can do something about disease tolerance if you breed the genetics in from one of the wild species of tomato.
DarJones
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joseph
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Post by joseph on Nov 5, 2010 6:08:50 GMT -8
I think you might be making an assumption that the genes for tolerance exist in the American Chestnut. And you are making the assumption after only 5 generations of exposure that suitable poly-genes don't exist.... The genes for resistance could come from any part of the genome or from many different parts of the genome... A different type of bark... A different clotting mechanism... A hypersensitivity... A modified life history... A population living in a different location such as China... etc... And as far as tomatoes go. In my garden tomatoes are essentially immune to all of the common blights that afflict tomatoes that are growing in other areas in which they are not well adapted. Besides all that, tomatoes only left their native range a few hundred generations ago. And at a 2% cross-pollination rate there might be as few as 6 actual exchanges of DNA in all that time. Again hardly long enough to say that "the gene doesn't exist". Besides horizontal resistance isn't about finding "The Gene". It is about little things adding up, like a slightly hairier stem, coupled with slightly more or less protein in the stem, coupled with a bit more or less wax excreted by the leaves, coupled with a slightly different sap chemistry, coupled with a different chloroplast, coupled with a slightly modified root, coupled with slightly different enzyme pathways, so that by the time all the slightlys are added together the plant is effectively immune to the disease even though it doesn't carry a gene for immunity. If I want I can plant a cactus in Hawaii and expose it to 2 inches of rain per day for every day of the year, but it hardly seems proper at that point to start badmouthing the cactus for not having genes for resistance to bacteria and mold.
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Post by DarJones on Nov 6, 2010 22:43:32 GMT -8
Tomatoes went through a genetic bottleneck during domestication that severely limited their diversity. This is very well documented and can be read about in several of Charles Rick's publications. The problem that a bottleneck causes is that diversity is reduced so significantly that a species becomes susceptible to being wiped out by diseases that would otherwise not be a problem.
By comparison, teosinte - a wild member of zea closely related to maize - has hundreds of millions of plants with a reserve of existing variations that make up as much as 3% of the genome. This is a huge reserve that permits it to adapt to most possible environmental changes. Maize is a bit more restricted, but overall carries much more variation than most other domesticated crops.
My point is that having a huge reserve of existing variations is highly desirable for domesticated plants.
DarJones
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joseph
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Post by joseph on Nov 7, 2010 0:24:12 GMT -8
Tomatoes went through a genetic bottleneck during domestication that severely limited their diversity. Now that we are aware of the bottleneck are any of the growers on this list breeding with wild tomatoes? It seems to me that in today's world of instant communication and easy travel that such genetic bottlenecks could be easily removed. Near my home a wild perennial watermelon relative has naturalized (Bryonia Alba). It has a narrow genetic base... I think it would be a great service to the natural world if someone brought enough seed from Europe or Asia to expand the genetic diversity here.
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Post by GunnarSK on Nov 7, 2010 3:39:06 GMT -8
Now that we are aware of the bottleneck are any of the growers on this list breeding with wild tomatoes? It seems to me that in today's world of instant communication and easy travel that such genetic bottlenecks could be easily removed. Breeding with wild tomato species definitely takes place, but not necessarily (or always) to improve disease resistance. The best known example is the work of Oregon State University, where the objective is to produce a tomato with high anthocyanine content for its colour (cf. OSU Blue), but maybe Tom Wagner or Darrel Jones is breeding with wild species to increase disease resistance/tolerance.
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Post by murgatroyd on Nov 7, 2010 13:49:30 GMT -8
Seems as if most of the sources on the net say Matt's Wild Cherry tomato is either wild or half domesticated. If true then its an easily obtained source. Maybe breed it with the largest beefsteaks to get an average sized tomato? Maybe that's wishful thinking.
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