Potato Famine Pathogen's DNA Deciphered

Scientists have sequenced the genome of the water mold that causes "late blight" disease in potatoes, tomatoes and other food crops. Genome scientist Chad Nusbaum describes the pathogen's unique genome, and explains why decoding it may lead to new ways to fight the blight.

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IRA FLATOW, host:

You're listening to SCIENCE FRIDAY from NPR News. I'm Ira Flatow.

Up next, modern science meets the famous Irish potato famine. You may have thought that the microbe that caused the devastation into all those potato plants died off with the famine over 150 years ago, but it did not. It's still around today and it's called late blight and it's still wreaking havoc on crops. But this time, it's wiping out whole fields of tomatoes. And the cold, rainy, spring and summer in the Northeast made for ideal conditions for this fungus-like organism to spread.

The good news is that the scientists now have a better understanding of the enemy the farmers are trying to fight. A team of scientists has sequenced the genome of the organism, also called a water mold, and gotten to look inside the arsenal it uses to kill its plant hosts.

And joining me now to talk more about it is Chad Nusbaum. He's the co-director of the Genome Sequencing and Analysis program for Broad Institute of MIT and Harvard. And he joins us by phone. Welcome to SCIENCE FRIDAY.

Dr. CHAD NUSBAUM (Co-director, Genome Sequencing and Analysis program, Broad Institute of MIT and Harvard): Thanks for having me on. I'm a fan of the show.

FLATOW: Thank you. You're welcome. Why did you choose this organism to sequence?

Dr. NUSBAUM: Well, I first met with up with the potato blight community about six years ago. I should say I'm not a plant pathologist. I'm a genome biologist, and it was sort of at the end of the human genome project. And I met up with the potato blight researchers. And the genome had not been sequenced at that time, largely because it was too big and complicated for the existing funding mechanisms for microbial genomes. And they got me interested in the project, and I said this is something that really needs to be done.

FLATOW: Mm-hmm. And why does this organism - is there some doubt about what it actually is being classified? People talked about it as a fungus. And I mentioned it was fungus-like.

Dr. NUSBAUM: Yeah. It's not a fungus. It's been called a fungus, you know, back to the days of taxonomy by anatomy because it looks like a fungus. Although even in the early days of doing microscopy on it, you could see that its spores were very different from fungal spores because they have flagella and they swim. Maybe in the middle of the last century, that is the 20th century, people started to realize that there were differences in cell walls, cell wall structure and sterol metabolism. So, there was clearly something different about these things. But they were studied by people who also studied fungi, and they did things like kill crops that fungi also do.

And round about 20 years ago, when people started using DNA sequence data to get a deeper understanding of tree of life, researchers began to understand that, well, there's a lot more to larger organism genomes than just plants, animals and fungi. In fact, there's a much greater variety than can be described by those three groupings. And, in fact, the water molds or the oomycetes - as they're now sort of scientifically called - fall in a group that's more closely - that's very differently related to fungi and more closely related to diatoms and kelp, and in fact, isn't too distant to malaria.

(Soundbite of laughter)

FLATOW: So, it don't really fit in anywhere?

Dr. NUSBAUM: Well, they do. They fit in a place that we didn't know about.

FLATOW: Sort of like the Pluto of funguses that's been reclassified.

Dr. NUSBAUM: Well, it's more like Kuiper belt because there's a lot of all that stuff out there past Pluto as well.

FLATOW: Uh-huh. And now that you have the sequence of this genome, can you actually figure out a way to attack it any better or can science find ways to do that?

Dr. NUSBAUM: Yes. And obviously, that's why we get into it. And one of the - a little careful not to oversell this. You know, in the history of genome biology, we sometimes been guilty of, shall we say, a bit too much enthusiasm…

FLATOW: No.

Dr. NUSBAUM: …about how quickly our data will have an impact. So, you know, our results won't immediately provide a tool to wipe out the pathogen, but what we do provide is a deep data set that shows you what's going on at the molecular level. In essence, it's a comprehensive parts list for the organism that's now available to plant pathology researchers. And we know where all the genes are or the vast majority of them. And we can start to study how they work in detail.

FLATOW: Does the genome tell you why it's such a potent killer and are tough to wipe out?

Dr. NUSBAUM: Well, the genome tells us a lot about why it's so aggressive in terms of evolving to overcome the plant resistance. And so, what happens is that the genome has - as we looked at the genome sequence, we see that it has a peculiar structure. First of all, the genome is substantially larger than that of other water mold genomes. And that is because it is full of these transposons - these transposon elements which are the sort of these parasitic genes - gene elements that jump around and copy themselves. And the genome sort of filled up with them and you might say to yourself or I might say to myself, but why should the pathogen bear the burden of carrying these things around since it's very expensive to replicate all that extra DNA?

And so how this connects to the pathogenicity or the aggressiveness of evolution of this organism is that the genome - if you look at the related organisms, you can see that most of the genes are the same and they're kind of in the same order, and they fall in the regions of the genome. The ones that are mostly the same, fall on the regions of the genome that don't have that many transposon to them. And these are sort of broken up by regions of the genome that are chock-a-block with these jumping genes, these parasitic transposons, and that's where a lot of the genes involved in pathogenesis are located.

And so now, what's happening is that these regions of the genome where - that are full of transposons and full of the - or where the pathogenic genes live, there are so many of these transposons that DNA replication starts to make mistakes and you duplicate or delete regions so that you start to add or subtract copies of the gene over the generations.

FLATOW: Uh-huh.

Dr. NUSBAUM: And so now you get my theory here that what's happening is that the pathogen has many hundreds of these genes, and it does this sort of constant making and destroying of these genes in a plant obsolescence kind of strategy so that the host plant can never keep up. And that you're sort of always modernizing your arsenal, and so you don't worry whether these genes work or not. You just keep them for a while and throw them away.

FLATOW: So it's mutating then.

Dr. NUSBAUM: Well, it's mutating but not - it's mutating, sort of, in the sense it's making new copies of genes and then those genes have a chance to evolve.

FLATOW: Oh.

Dr. NUSBAUM: And then it's also throwing them away at a rapid rate.

FLATOW: Mm-hmm.

Dr. NUSBAUM: So this is - I sort of have this theory that it's almost domesticated or partially domesticated. These transposons for the purpose of giving it an evolutionary speed advantage. We call it the two-speed genome. The sort of normal part of the genome is evolving like most genomes, and the two-speed part where you're making and losing these weapon genes very rapidly.

FLATOW: So it would be to the fungus' - let's call it that - advantage to keep this process going?

Dr. NUSBAUM: Well, I think so.

FLATOW: Yeah.

Dr. NUSBAUM: You know, as an evolutionary biologist, I always think it's -something is kept around for long enough. It might be there for an advantage reason.

FLATOW: Mm-hmm. Are there other pathogens that work the same way?

Dr. NUSBAUM: Not that we know of. It's likely that there are other genomes behaving the same way, but we don't know of anything that is moving at this rapid rate.

FLATOW: Wow. So that's what makes it all so interesting to study.

Dr. NUSBAUM: Well, it was a quite a challenge to study. It seems that everything you do with this organism is tricky. It was very difficult to make a genetic map of it. But it was very difficult to put the genome together because it had so many copies.

FLATOW: Mm-hmm. And…

Dr. NUSBAUM: And it's difficult for the agricultural sector to deal with.

FLATOW: Yeah. It's not to say there are not insecticides, herbicides that can deal with it, or fungicides. Well, what kind of cide(ph) would we call it?

(Soundbite of laughter)

Dr. NUSBAUM: Well, one of my…

FLATOW: It's not really a fungus. What do we call it then?

Dr. NUSBAUM: One of my colleagues once suggested calling them oomycetecides(ph) because they are oomycetes, but the name never really stuck. So they call them - there are chemicals that work on them and they call them fungicides, really, for a couple of reasons. One is that some of the things that work on them also happen to work on fungi, and then the ones that do work against the oomycetes -it's just easier to call them fungicides.

FLATOW: Mm-hmm. Do you have another challenge you're going to be working on next?

Dr. NUSBAUM: Well, one of the challenges I'm interested in doing is I want to understand more about the fast evolution of these genes, and the way to do it is too look at genomes that are very closely related.

So we've got a project that we've mapped out and that we're trying to raise money for so we can sequence a bunch of closely related species that have different host ranges with the notion that if we can capture these genes in the process of evolution, you know, as they're appearing and disappearing, and correlate that with changes in host range, we can learn a lot about the mechanism of how that works.

FLATOW: And how fast do they appear and disappear?

Dr. NUSBAUM: Well, we don't know that because we haven't looked closely enough. The distances that we see with the genomes that we're looking at are fairly far apart. All we know is that they're moving faster than we can tell.

FLATOW: Uh-huh. Does that mean…

Dr. NUSBAUM: They're moving way faster than regular genes.

FLATOW: Are we talking months, weeks, years?

Dr. NUSBAUM: No. I mean, many years.

FLATOW: Many years.

Dr. NUSBAUM: But still on the evolutionary time scale, it's pretty fast. We have some anecdotal evidence of individual events, but it's not enough to put a real time, a real rate on the process.

FLATOW: And do you know specifically what some of these attack genes are actually doing?

Dr. NUSBAUM: So we know for example that there are sets of these genes that a pathogen will secrete onto the plant cell because it doesn't penetrate plant cell. And that these have little signals on them that are coded to have them be taken up into the plant cell.

And for some of these genes, we've - in the summer, this is on a recently published work, we've taken apart the genes and we can see that we can identify the domain in a gene - are the domain in the protein, the piece of the protein that's responsible for killing the plant cell when we get in there.

There are lots of other pieces of these genes that we don't yet understand what they're doing. But as I've said, a recent work gives us a parts list so we know what to start taking apart.

FLATOW: Mm-hmm. So it doesn't grow in the plant, let's say, a tomato plant that it's attacking.

Dr. NUSBAUM: Well, it doesn't grow inside the cells. It kind of grows between the cells and kills them. And it sucks up the juices.

FLATOW: Yummy.

(Soundbite of laughter)

FLATOW: And that's a little different than the way a fungus operates.

Dr. NUSBAUM: Well, some fungi actually penetrate into the cells, yeah.

FLATOW: Yeah. So this - can you look at a plant and say, uh-oh, this is that gene working. This is that - uh-oh, not the fungus working?

Dr. NUSBAUM: Oh, yeah. You can definitely look at the leaves and say this is likely to be a late blight infection, sure.

FLATOW: Mm-hmm. And do you have any…

Dr. NUSBAUM: I saw, in fact, that wasn't - maybe a few weeks ago, I was at a friend's house for dinner and she said, go out in the yard and pick some tomatoes. I have some lovely ones out there. And I went out there, and from 10 feet away, I knew we weren't going to be eating those tomatoes.

(Soundbite of laughter)

FLATOW: So you could look at them and see the fungus or they…

Dr. NUSBAUM: Well, the leaves had this sort of brown edges and were curling up. And when I got closer, they had these lesions and the ends of the tomatoes had all gone black and yucky.

FLATOW: Well, it's funny that you bring that up because that's exactly what our - you're leading us in to our Video Pick of the Week this week is that Flora Lichtman, who's here now. Hi, Flora.

FLORA LICHTMAN: Hi, Ira.

FLATOW: Meet Chad Nusbaum.

LICHTMAN: Hi, Dr. Nusbaum.

Dr. NUSBAUM: Pleased to meet you.

LICHTMAN: Thank you.

FLATOW: Flora actually went out to one of these fields. And on our Video Pick of the Week up on our Web site at sciencefriday.com, shows you what an attack of this non-fungus can do.

LICHTMAN: Yeah, it's pretty gruesome. I mean - I think - I was surprised at just how bad those tomatoes look when they have late blight. I certainly don't want to eat them. They have these kind of giant, greasy patches on them.

FLATOW: Chad, (unintelligible) you call it greasy yourself, but…

Dr. NUSBAUM: Yeah, they do look greasy or slimy. Yeah - my - a friend of mine who runs an organic farm in the next town over from where I live emailed me and said, come see the devastation. She said you can smell it.

(Soundbite of laughter)

FLATOW: We're talking about tomato blight, I call it, this hour in Science Friday from NPR News with Chad Nusbaum and Flora Lichtman.

So tell us, Flora, what you did. You went out and video this field of stinking tomatoes.

LICHTMAN: Yes, Annette Heiss(ph) and I went out to eastern Pennsylvania to Tim's Stark's farm, Eckerton Hill Farms. And he's a tomato man. That's how he describes himself. He has 25,000 tomato plants in the ground. And, you know, he was in this situation this year and he said, he just felt it in his bones. He knew late blight was going to come on because of the unseasonably cold and rainy weather.

And then, it sounds like there's - you know, on top of that weather which promotes the blight, there was also this added thing with the big box stores selling infected plants to home gardeners, who couldn't really - who didn't recognize that this is late blight, so there was a lot of pathogen in the air. Is that - Dr. Nusbaum, is that your impression of…

Dr. NUSBAUM: Yeah. That's exactly as I understand it. And you said that the home gardeners didn't recognize it. Not only do they not recognize it, but, you know, a farmer would see this and they know just what to do. They cut the plants down and brown bag them, or black bag them, so the pathogen would dry up. But what the home gardeners did is they hung on as long as they could to try and get some tomatoes and then - of course, that should've kept the blight going.

LICHTMAN: Right. And so - then you have all these farmers who are in the situation, and it's compounded by the weather. And I think for this particular farm owner, Tim Stark, who, you know, runs a farm basically organically. He's not certified organic, but he doesn't use pesticides or fungicides or oomycetecides.

(Soundbite of laughter)

LICHTMAN: And he was in the situation this year where, the - basically, his livelihood depended on spraying, and ultimately that's what he had to do.

FLATOW: So your video shows how he reluctantly had to pull out the sprayer.

LICHTMAN: Yes. He reluctantly pulled out the sprays. And he seemed to really be pretty torn up about it. And he said that actually at the farmers market where he sells in New York that some people completely understood, and other people really just turned around and stumped off when they found out that he sprayed this here.

FLATOW: Chad, have you seen this widespread - this because of the raining, cool summer we had?

Dr. NUSBAUM: Yeah, and that's exactly what from talking the farmers I've heard as well. Very ideal weather for the blight. They call it the late blight 'cause it usually comes on late in the season. There's another pathogen called the early blight. But because - and it loves cool, wet, windy weather which as Flora said, that's exactly what we were facing all over the Northeast this year. And it…

LICHTMAN: And is that because they can swim? Is - I mean, that there's…

Dr. NUSBAUM: Yeah.

LICHTMAN: They can…

Dr. NUSBAUM: The spores swim. They're not airborne. They need to go in water. And they have these little flagella. In fact, they have two flagella. And one of the flagellum is different from the other, which is very strange.

FLATOW: So they swim from plant to - if you get them wet, they'll go to the next plant.

Dr. NUSBAUM: Well, they're sort of carried in the water droplets and then when they get on the leaves, they swim until they find the right place to infect.

FLATOW: Wow.

LICHTMAN: So that's why the rainy weather was a key, I guess.

FLATOW: Mm hmm.

Dr. NUSBAUM: Well, weather is great for them.

FLATOW: So what's the right way to destroy these plants if you have them?

Dr. NUSBAUM: Well - so, the right way to do it - and this is what my friend, the organic farmer did is as soon as their tomatoes got infected that you cut them down and you put them in these black plastic bags and leave them in the sun to dry out. And the other thing that's sort of interesting is, it's actually and even more severe pathogen on potato.

And she said, as soon as she saw it on her tomato, she cut the green part of her potato plants down to the ground, and that allowed her to salvage a fair amount of the crop, the tubers were smaller, but at least the crop wasn't destroyed.

LICHTMAN: Tim Stark did the same thing. He forked out all his tomatoes - oh, sorry, his potatoes before they got infected.

FLATOW: Mm -hmm. Well, and let's see this time, as opposed to Ireland 150 years ago, we do have a backup which is a fungicide that'll kill the blight.

LICHTMAN: Great.

FLATOW: Now, thank you, Chad, for taking out…

Dr. NUSBAUM: Well, (unintelligible) pleasure.

FLATOW: You're welcome. Chad Nusbaum is a co-director of Genome Sequencing and Analysis program for the Broad Institute of MIT and Harvard. And Flora, thank you.

LICHTMAN: Thanks.

FLATOW: Our Video Pick of the week - if you like to see this really amazing blight and the video that Flora made, it's up on our Web site at sciencefriday.com. And it's really amazing how devastating this thing really is.

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