Breeding for Late Blight Resistant Tomatoes

[reed]

My personal aim is to make neglectable tomatoes.

I guess mine are sort of that, I wish I could let them sprawl on the ground, but I don't have room for that. 

If it were me I would at least carefully save some seeds for the future so that if they do cross I could always go back to pre-crossed material if necessary, such as if/when PH-5 is overcome.

Absolutely! I have lots of backup seeds.

That's curious, from what I remember that's PH-2 and PH3 homozygous so should be among the very best LB resistance. But I guess maybe if it did that early, it wasn't LB. I wonder if it was the same issue which Julia had with hers and had assumed was LB?

Could have been, sometimes it's easy to jump to conclusions. I have several tomato diseases in my garden, I've never bothered to positively identify them. 

The LB resistant ones you grow now, were they showing such resistance before you (or neighbours) ever grew commercial LB resistant varieties, or, only after? And from what I remember, one of your LB resistant ones is the one you refer to as 'my Mr. Stripy' - is that different from other people's Mr. Stripy?

I had Mr. Stripey years before I ever heard of late blight. Also, Cherokee Purple but it isn't as tolerant as Mr. Stripy. Oh yea, almost forgot the pimps only I always called them currents, I've had them a long time too. The others in my pictures I've gotten more recently.

I don't know if my Mr. Stripey is the same as others by the name or how many go by it, but I suspect maybe yes, and no. Nobody else I know of grows it except from my plants, never seen it at farmer market but you can buy it by that name.

I have a goofy theory that all the Mr. Stripy - like tomatoes are probably related and linked to some that came back from Europe into the Appalachian Mountains and spread from there. That's why I got that new one Willard Wynn, this year to see how it compared. It did well enough, I'm growing it again next year. I'm going to get two or three more nest year. I also have another called pineapple, very similar but not productive at all. Pineapple, at least the one I have is nicely tolerant, Willard Wynn had some variation, which I found surprising and of course Mr. Stripey. I want to find more of them that fit in with the group and maybe try to cross them with each other.

I think it might be a situation somewhat peculiar to my garden, but I can't really explain it. It is strongest but it doesn't apply to just the Mr. Stripy. I only got Utah Heart less than ten years ago and what I call Hoosier Rose about the same time, and they do fine, they replaced others I had had for decades.

[Cathy A]

"My personal aim is to make neglectable tomatoes."

This is one reason why amateur breeders are still important.

Commercial breeders are going to focus on maximum yield when treated in a very specific, carefully controlled environment with lots of commercial pesticides and fertilizers.

[William Schlegel]

I think a segregating population should be perfect for keeping multiple genetics like PH and non PH tomatoes as long as it is large enough. The only 2023 cross I made with Reeds with PH genes was 1/4 purple Zebra F1. So even in the F1 only some of them will pick up those genetics.

I have been pretty obsessed with bicolor tomatoes like pineapple and mr. Stripey. If it is a related group I've been personally doing my duty to make it more diverse at the genetic level. Though I think I found some new good ones in other colors. Some of the green when ripe are way better than I thought.

[reed]

I have been pretty obsessed with bicolor tomatoes like pineapple and mr. Stripey. If it is a related group I've been personally doing my duty to make it more diverse at the genetic level

We love the bi-colors or tricolors. Any combination of red, orange, yellow, in swirls or streaks. There are bad ones, like tigerella, but the big juicy ones with soft tender skin are just about all good. Differences are mostly in general stress tolerance and level of production. Green ones are ok too but haven't found one as tolerant or productive as the yellow.

I need t go back through the thread and find those that were being discontinued, and that link to those old paintings.

 

[Cathy A]

Justin, there may be some issues with Raoul's exact language in the book, but the overall concept made sense to me.

Instead of looking for specific alleles that given a great deal of protection against a very specific disease organism, the idea of horizontal resistance (it seems to me) is to look for genes that make the plant generally stronger, more resistant to any infection, and better able to survive the impact of any disease.

In practice, this just means that you grow your varieties in your garden where you have disease issues, and each year select the ones that do best.

The most controversial part is where he suggests culling plants that show 100% resistance to a specific disease. But I understand where he's coming from. It would be difficult to develop the plant's overall background resistance to infection if a few genes are providing so much protection that no selection is taking place on the rest of the genome.

Perhaps another approach would be to refrain from culling resistant plants, but grow them and select in an environment with a lot of disease pressure from many diseases, not just one or two. Then even the plants with disease-organism-specific vertical resistance will be undergoing selection because of the presence of other diseases.

[Justin Jardinier]

Justin, there may be some issues with Raoul's exact language in the book, but the overall concept made sense to me.

I can't judge the book as a whole as I just read that chapter on horizontal resistance and a bit surrounding it. To me, the concept sounded nice. I just didn't see it grounded in any kind of evidence or examples, which implies to me that much of what he was saying may have been fantasy.

Instead of looking for specific alleles that given a great deal of protection against a very specific disease organism, the idea of horizontal resistance (it seems to me) is to look for genes that make the plant generally stronger, more resistant to any infection, and better able to survive the impact of any disease.

Is there much difference in genes and alleles? Also I wonder, if one person has a plant which is resistant to late blight, and calls it horizontal resistance, then another person does some genetic analysis and find it is because of two genes, is that now vertical resistance because the genes have been identified? Of course my question is a little absurd, but that is not entirely by accident.

Also while the idea of plants having genes making them resistant to any infection is naturally very appealing to me, the species of tomato most renowned for disease resistance that I know of, is S. peruvianum. And I grew quite a few different accessions in my garden this year. They did great! Until, that is, late bight came, and it killed all of them. It also killed my various pimp accessions.

This was a bit of a surprise to me. But this is also what made me interested in specific genes, because so far as I have been able to discern, the only resistance I have heard of that can withstand heavy late blight such as we get here, is in/from some specific pimp accessions, and some specific habrochaites accessions. And I have not heard of anyone bringing that resistance over from hab. And, the genes responsible for that resistance in pimp have been identified, and are readily hereditable.

The most controversial part is where he suggests culling plants that show 100% resistance to a specific disease.

Yes, that sounds absurd to me. For example, suppose he were given a bunch of unidentified F2 tomato seeds that had a parent that was homozygous for PH-2 and 3. He would get some plants that would be homozygous for both, some heterozygous for both, some homo for one, hetero for the other, and so on through all the combinations. Suppose those homozygous for both showed no signs of late blight in his garden, which is quite likely - he would eliminate them! Even those heterozygous for both or hetero for one, homo for the other, might show no signs of blight! So throw them out too. So he may end up with some lines that have none at all, and maybe do not too bad in some seasons if he doesn't have much LB, and some others that do well stabilizing as homozygous for just one, which may end up being PH-2 since depending on conditions, PH-3 might be 'too good' for him! Plus, rather ironically, it sounds like he would call PH-2 + 3 homozygous 'vertical resistance' because in this scenario it would give total resistance, and PH-2 homozygous 'horizontal' because of only partial resistance, which might be rather embarrassing when it was revealed to him that his 'vertical' one was 'inherited polygenically' (which is in accordance with his definition of horizontal) and his 'horizontal' one would be due to a single gene!

So this method would lead to significantly inferior resistance, and also that resistance wouldn't last as long, as LB evolves. Plus even if he called it 'horizontal resistance' because it was only 'partial', once LB would overcome that resistance he would then say it was in fact never 'horizontal', because he defined horizontal as eternal, never possible to overcome (which so far as I understand evolution, is effectively impossible anyway).

Presumably he would also throw away hab LA1777 since that has total resistance, in many cases anyway. And if those wild pimps that are the source of PH genes never showed LB in his conditions, he should throw them away too!

If we extend this further, why not throw away all peas and carrots and wheat, because that has 100% protection against LB also! I find that logic ... illogical.

It would be difficult to develop the plant's overall background resistance to infection if a few genes are providing so much protection that no selection is taking place on the rest of the genome.

I'm not convinced by that. Are carrots and peas and wheat unable to develop 'overall background resistance to infection' just because they are 100% protected against LB? Or ... I do not know the specific details so let's take this as a hypothetical - suppose a vigorous wild population of S. peruvianum has total protection against Cladosporium leaf mould, or ToMV - do we then discard it, and assume that it must be generally unhealthy, and that it can only hope to get 'overall background resistance to infection' if we breed out that resistance such that it becomes susceptible? I cannot imagine that being wise or true.

I'm not totally dismissing the idea. But so far, exploring it logically, and trying to ground it in realistic examples, has in my mind seemed to show that it doesn't make any sense.

Perhaps another approach would be to refrain from culling resistant plants, but grow them and select in an environment with a lot of disease pressure from many diseases, not just one or two.

Yes that seems like a logical way to breed. My idea is to breed in the area the seeds are intended to be used. So that they get to be selected for the diseases they will encounter later, which I suppose has been the standard way of breeding for the entire history of agriculture aside perhaps from some modern commercial breeding, involving deliberate gene stacking. Though I would expect they also test through their process, in the conditions they mainly sell for (which is disadvantageous to us if we live in different conditions, or if they breed for mainstream toxic agriculture and we grow organic, or they breed for commercial greenhouses and we grow outside). But they would also deliberately infect plants, and I really like that idea too. If possible I would like to not merely expose my plans to the diseases as they naturally arrive in the environment, but also to LB in some seedling trials, to save time and space. If they do badly against LB, it doesn't really matter to me if they do well against something else, or even everything else! Because there are plenty of tomatoes that do well in a season with no LB, but LB resistance seems to be the weakest link. So I would sooner eliminate everything that doesn't do well against it, and then expose the rest to the natural conditions, with as little pampering as possible, so that they can be further selected for all that. And for sure those which show no LB at all with be the most prized on that metric, won't be throwing those away!

Another thought that just occurred to me is a questioning of the concept 'overall background resistance to infection' vs 'resistance to a specific disease', by the example of diseases that Europeans, even if relatively unhealthy, could deal with fine, but people in the Americas or Australia died very easily from, even if they were healthy and their general level of immunity was very high. This relates to me to the case of peruvianum, which is so famed for its resistance to disease, and yet is so susceptible to LB. As well as to some domestic tomatoes that may be so very healthy and productive, until LB comes. And the fact that various accessions of pimp might seem to have equally wonderful general disease resistance and environmental stress tolerance, and yet when exposed to LB, some will die and those lucky enough to have those resistance genes, do fine.

Another example is Joseph's tomatoes. I think the BH line has some resistance to LB (though seems not enough for those of us with heavy LB), but the others generally seem to do very poorly against LB. I suppose I am repeating myself now, but I give them as an example of tomatoes with very diverse genetics, that do very well in Joseph's area and I'm sure in some other areas too. Like with the wild species I have grown, it seems merely being generally good or healthy, is not enough. Also I just remembered that peruvianum has been grown in Europe since... ok I'm a bit lazy now, I know it's a very long time but forgot where I read it, so I asked chat GPT and it claims since the 18th century - might be right. And it's an outcrossing species so evolution should be relatively quick. And yet, apparently that's just not enough. I know of no peruvianum that has resistance against LB.

[William Schlegel]

I think long term climate might be more important to late blight and needed level of resistance than other factors.

If late blight was really a threat to all tomatoes, then all tomatoes in its natural range as a pathogen would have higher levels of resistance to it.

So I suspect areas like the pacific Northwest of the US, the Eastern US and Europe are where LB genes are most needed. I can cross in LB resistance genes but unless LB gets worse here genetic drift will continually erode its percentage in my tomato populations.

[Nicolas]

I'm still a bit confused by horizontal vs vertical resistance.

At a definition level, vertical resistance is based on a gene on gene relationship, similar to a key to lock matching. Either the plant is resistant wrt a pathogen genetic (100% resistance), either not (0%).

But modern breeders dont care about vertical vs horizontal resistance, they select for high heritability, thus (co)dominant genes with powerful effect, for ease and feasibility of pyramiding/staking resistances in parents and with F1.

Ph-X genes from pimpi are partially dominant, with significant effects, and resistance depends on LB strains.

QTLs from habrochaites are recessives, with significant effects but not as much as Ph-X it seems (difficult to have some data)

I guess one could determine if Ph-X resistance is vertical by looking at mechanisms at stake. Either it is genetically oriented, or not (such as physical features that could provide some indirect advantage)

The know thing is that it is difficult to stake Ph-X genes without markers because only one or two genes are sufficiant to provide max natural selection benefit from LB.

[Justin Jardinier]

At a definition level, vertical resistance is based on a gene on gene relationship, similar to a key to lock matching. Either the plant is resistant wrt a pathogen genetic (100% resistance), either not (0%).

By that definition, that would make a single PH gene 'horizontal', since it only gives partial resistance. And yet that contradicts Raoul's definition that it is eternal - PH-1 has already been overcome.

QTLs from habrochaites are recessives, with significant effects but not as much as Ph-X it seems (difficult to have some data)

I guess so long as they're homozygous, that's not a problem right? But I guess it would take a lot of breeding to get all the genes responsible over to a new population.

Are you sure the LB resistance of hab LA1777 is not as much as the PH genes? My impression was that it's stronger, I thought. My only direct experience is that I grew heterozygous PH-2+3 this year and it did finally get LB, and I grew one plant of LA1777 and it seemed to get no LB at all, and even after the first 0C temperature it survived, with some leaf damage. I had a couple of Joseph's hairy habs and they did very well too, but looked like they got a bit of LB on their stems, and did not survive the freeze - a close second best though. A few of a non-hairy hab, they got LB. And a slightly hairy hab that was nicely early, initially did great against LB while the domestics and peruvianums etc were dying, but, finally did seem to get it, and died, though produced plenty of fruit beforehand - if the resistance of this one is hereditable it still might be useful perhaps. LA1777 was amazing though, seemed totally untouched.

So I can't compare it via personal experience with homozygous PH anything, and I don't remember specifically from papers seeing them compared, but, I had thought that was the case - I might be wrong though.

The know thing is that it is difficult to stake Ph-X genes without markers because only one or two genes are sufficient to provide max natural selection benefit from LB.

I've seen tests in papers and by a member of this forum, I think it was Roland? where plants were tested by being infected with LB, and it was really clear that PH-2 + 3 homozygous was more resistant than any other combination of PH-2 + 3 or by themselves. It was also clear that having both was better than 1, and from what I remember that 3 was better than 2, though I don't know if that applies to every strain of LB. Basically the gradient in the combinations was evident. So this seems a really good way of enabling us to stack the genes without the need for markers.

On the other hand, since PH-2 + 3 homozygous gives such strong resistance, we might need markers if we want to additionally stack PH-5. And I don't know how PH-5 compares to the others exactly, but from what I remember it itself is a combination of 2 genes on different chromosomes, and is stronger than 2+3 homozygous. So, let alone having all three PH resistances homozygous, we might need markers to get any additional ones added to PH-5. That's why I was thinking about keeping PH-5 separate, so could aim to get PH-2+3 homozygous population and separate PH-5 population just via infection trials. Though for an outcrossing population it does sound cool to put them all in the mix and hope for the best.

[Joseph Lofthouse]

I fully embrace Raoul's stance of eliminating alleles that have a huge QTL for disease resistance. I would rather gather together 100 alleles that contribute 1% resistance. That explains why I am not working on stacking resistance genes into a single variety. In my own life, I'm not going to discount his work by approaching it with black/white thinking. Saying that he has to be wrong, because the QTL of a resistance trait is actually 90%...

Is there much difference in genes and alleles?

In the case of the self-incompatibility trait in tomatoes, the s-gene has about 35 alleles, meaning that there are about 35 variations of one gene.

[Joseph Lofthouse]

The most controversial part is where he suggests culling plants that show 100% resistance to a specific disease. But I understand where he's coming from. It would be difficult to develop the plant's overall background resistance to infection if a few genes are providing so much protection that no selection is taking place on the rest of the genome.

I have come to believe that adaptation agriculture selects for plants with a general resistance to stress, regardless of whether that stress is biological, or related to soil/climate. A plant that thrives in it's ecosystem resists late blight better than a plant that struggles to eke out a meager existence.

[Nicolas]

By that definition, that would make a single PH gene 'horizontal', since it only gives partial resistance. And yet that contradicts Raoul's definition that it is eternal - PH-1 has already been overcome.

I think Ph-X are vertical, because Ph-1 worked very wel but is now useless. Ph-3 is 100% tolerant on the US studies i've came across. And it seems that Ph-2 has been broken. Some strains have broken Ph-3 too.

Are you sure the LB resistance of hab LA1777 is not as much as the PH genes? My impression was that it's stronger

Yes LA1777 is stronger, it is each individual resistance genes that are weaker that any Ph-X. LA1777 has at least 5 QTLs, but i've seen no data about each QTL power.

I've seen tests in papers and by a member of this forum, I think it was Roland? where plants were tested by being infected with LB, and it was really clear that PH-2 + 3 homozygous was more resistant than any other combination of PH-2 + 3 or by themselves. It was also clear that having both was better than 1, and from what I remember that 3 was better than 2, though I don't know if that applies to every strain of LB. Basically the gradient in the combinations was evident. So this seems a really good way of enabling us to stack the genes without the need for markers.

From my understanding on US studies, it is not possible to deduce Ph-X genes from resistant plants, it could be Ph-3/Ph-3 or Ph-3/+ Ph-2/+ or stronger combinations. Could be different in EU depending on strains.

[William Schlegel]

Has anyone read the 2012 edition of Return to Resistance? Molecular evidence may have caused a lot of revision by then. Has anyone done a literature search? Maybe there has been a even more recent thesis or review of the ideas that could help reconcile these concepts. I would expect subtle intergradation between the concepts. Otherwise why would different types of resistance genes be conserved by adaptation over deep time?

It would make sense to me if traditional indigenous gardening and farming of tomatoes maintains a balance with pathogen and crop. Possibly partly because of occasional outcrossing. I think that might be Gary Paul Nabhan's influence though. I would expect to find great variation in resistance in traditional tomatoes from Mexico south to Peru but also may be less than we would think because of the balance achievable through variation.

Uniformity in my view is what makes resistances quickly obsolete. Large fields of the same crop variety.

[reed]

I have come to believe that adaptation agriculture selects for plants with a general resistance to stress, regardless of whether that stress is biological, or related to soil/climate. A plant that thrives in it's ecosystem resists late blight better than a plant that struggles to eke out a meager existence.

I figured that out a long time ago and see evidence of it all the time. Non-scientific evidence, I have not done trials of one process compared to another or even kept good documentation showing comparisons over time. What I do see and hope to continue seeing is a consistently adequate for our needs harvest, regardless of what stressors are most prevalent that season, and with minimal effort on my part.

I know little about the specific genes involved in much of anything and am not really all that concerned with what diseases might or might not be present. I don't fertilize anything; I don't treat anything and very rarely even water anything. If something fails to produce the adequate for our needs harvest for whatever reason, I drop it. A total failure in one year results in permanent banishment, even if there is a chance, it might thrive the next year, I have no problem with a small harvest due to adversity, but no harvest is a deal breaker. The conversation goes sort of like this. "I know you had a bit of the brown curly leaf disease; the big green worms ate some of your healthier branch tips, then you had touch of the grey fuzzies, and then it didn't rain for five weeks but still, you could have given me a tomato or two, and you didn't. I'm sorry but I'm afraid I have to let you go." 

Good enough is good enough for me and adequate for our needs, is good enough but I want it every year. I'm also of course not displeased when a harvest exceeds that, as is often the case. I wouldn't rule out however that I may set the bar lower than many people.  I'd rather expect less and be happily surprised than stress out over wanting more.

It would make sense to me if traditional indigenous gardening and farming of tomatoes maintained a balance with pathogen and crop

I don't know about the indigenous, but I think that is basically what goes on in my garden and although some varieties like my Mr. Stripy have been growing here for thirty years, that deeper time association with whatever is going on isn't necessary. Utha Heart from Joseph and Hoosier Rose from a commercial source both took right to it while many others did not. I can only guess from that, that there is genetic component. Some tomatoes, no matter where they come from or what genetics they are supposed to have settle in here just fine, even though most don't.  I speculate that there is some magic combination of genes in some tomatoes that works this way but don't expect I'll ever know what that is. And maybe it's not just one specific combination. Maybe there is more than one, maybe a different one would work better somewhere else.





   

[Cathy A]

"Has anyone read the 2012 edition of Return to Resistance?"

My copy is 3rd edition, 2007. I wouldn't expect huge differences in the 4th edition.