Plant-Pathogen Interactions

Part 1: Introduction to Plant-Pathogen Interactions

00:00:07;13 Hi, I'm Sheng Yang He.
00:00:09;13 I'm a professor at Michigan State University.
00:00:11;09 And I'm an Investigator of the Howard Hughes Medical Institute.
00:00:14;27 Today, I'm going to tell you about the
00:00:17;09 fascinating world of plant-pathogen interactions.
00:00:20;12 Now, why do we care about plant-pathogen interactions?
00:00:23;11 Some of you may know a disease called potato late blight.
00:00:27;23 This disease devastate...
00:00:30;19 devastated the potato crop in the 1840s in Ireland.
00:00:36;04 That event basically killed about a million people,
00:00:42;18 and another million emigrated... forced emigration...
00:00:47;15 out of Ireland.
00:00:48;24 Many of them actually ended up in the United States.
00:00:51;02 So, this just illustrates how a plant disease
00:00:53;26 can have a profound effect on human survival and emigration.
00:00:59;02 There are many such diseases, not to this scale,
00:01:02;18 but they are major threats to our global food securities.
00:01:05;19 So, one of the other diseases, you know,
00:01:07;29 like rice blast, I grew up with in China.
00:01:10;04 I lived in a small village,
00:01:12;17 and it was very severe when I was growing up.
00:01:15;13 But, you know, now I go back 40 years later.
00:01:18;21 It's still a very severe disease.
00:01:20;22 In fact, this is the number one disease in rice production across the globe.
00:01:24;21 There also are new diseases like kiwi bacterial canker,
00:01:28;22 which is caused by a bacterial pathogen that I'm very familiar with
00:01:31;26 called Pseudomonas syringae,
00:01:33;05 sweeping across New Zealand and some European countries right now.
00:01:37;09 So, you see there are old and new diseases.
00:01:39;26 They really pose a great threat to agriculture.
00:01:42;26 And so the... many researchers are, you know,
00:01:45;28 involved in trying very hard to understand the molecular basis of these diseases.
00:01:51;08 And the goal is to... hopefully, to come up with
00:01:55;13 very innovative solutions to solve all these diseases.
00:01:58;22 It's been very challenging.
00:02:01;10 But I think, you know, this is an area that we have to do,
00:02:03;28 because the crop production has to increase
00:02:06;22 to meet the demand of the rising population in the next century, actually.
00:02:12;16 So these diseases are one of the obstacles
00:02:16;26 to increase the yield production.
00:02:18;20 And also quality... you know, disease affects quality as well.
00:02:22;14 And so, in today's... this part of my talk,
00:02:25;29 I'm going to introduce some of the very general concepts
00:02:28;26 dealing with host-pathogen interactions.
00:02:31;19 On the one side, I'm going to talk to you about plant immunity.
00:02:35;06 Yes, plants do have immune responses like a human.
00:02:37;15 But I also want to talk about pathogen virulence factors
00:02:40;29 and so-called effectors.
00:02:43;08 That's Part 1.
00:02:45;19 In Part 2, I'm gonna illustrate these concepts
00:02:48;22 using the model Arabidopsis-Pseudomonas syringae system
00:02:53;04 that we and many others are actually working on.
00:02:55;02 So, I hope you're able to watch both parts,
00:02:57;22 because if you only see one you may not get enough information
00:03:02;03 from this talk.
00:03:04;09 So, what is effector-triggered immunity in plants?
00:03:06;16 There's an older name for this.
00:03:08;19 This is called, actually, gene-for-gene resistance.
00:03:10;23 This is describing a phenomenon, probably noticed by farmers or by,
00:03:15;09 you know, other people, over many years, thousands of years, probably.
00:03:19;03 You know, if you go into the wheat field
00:03:21;15 where there's different cultivars that are planted,
00:03:23;24 some cultivars will be severely diseased in some years.
00:03:27;12 And at the same time, some cultivars will be green and,
00:03:29;24 you know, yielding really well.
00:03:31;15 What's the molecular basis of that?
00:03:33;04 What's the genetic basis of it?
00:03:34;19 And that's been, you know,
00:03:36;00 puzzling for many people for a long time, until this scientist named H. H. Flor.
00:03:42;13 He's a plant breeder and a plant pathologist.
00:03:45;06 He studied a disease called the flax rust disease.
00:03:49;08 It is caused by a fungus.
00:03:50;24 He was very careful.
00:03:52;15 He studied many strains of fungal pathogens,
00:03:55;07 but also many cultivars of the flax plant.
00:04:00;18 And he studied the genetics of the interaction,
00:04:04;07 and came up with this very interesting hypothesis called
00:04:07;02 the gene-for-gene hypothesis.
00:04:09;05 What he thought is that maybe the pathogen
00:04:11;22 has so-called avirulence genes, or Avr genes, some strains.
00:04:15;20 And some cultivars that are resistant
00:04:18;02 contain so-called resistant genes, or R genes. Okay?
00:04:21;10 So, this is the diagram he would use to describe these interactions.
00:04:26;12 If he'd taken a pathogen without any avirulence genes,
00:04:29;06 it's going to infect the plants
00:04:31;27 that either have the R genes or no R genes, right?
00:04:34;13 Because it's virulent, okay?
00:04:36;02 But, if when the pathogen has Avr genes within it,
00:04:39;14 it's going to only infect the plants
00:04:43;01 with no corresponding R genes, okay?, which is depicted right here.
00:04:47;18 If the plant has R genes that can recognize genetically this Avr gene,
00:04:50;26 then the plant will be resistant.
00:04:52;27 So, you needed both the R genes in the plant
00:04:55;09 but also Avr genes in the pathogen
00:04:57;17 for a plant to be resistant.
00:05:00;20 So, this has... you know,
00:05:02;27 was a hypothesis only, okay?
00:05:04;19 But about 10 or, you know, 15 years later,
00:05:07;17 there's actually molecular proof for the existence of these interactions.
00:05:11;20 So, scientists started to clone these so-called Avr genes
00:05:17;11 from different kind of pathogens.
00:05:18;21 The initial few Avr genes were actually cloned from bacteria.
00:05:22;20 And this was done by Brian Staskawicz at UC Berkeley
00:05:25;05 and the late Noel Keen at UC Riverside.
00:05:29;03 And then about ten years later,
00:05:30;25 a number of R genes have been cloned from plants,
00:05:34;21 from different plant species.
00:05:36;15 Okay?
00:05:38;09 So, there were some original predictions of how the Avr proteins and R protein
00:05:41;13 would work, actually, right?
00:05:43;00 So, the idea was really inspired
00:05:45;11 by an animal receptor signaling kind of model.
00:05:49;12 It says that, you know,
00:05:51;03 this Avr protein may be made in the pathogen
00:05:53;15 but is secreted outside of the bacteria. Okay?
00:05:56;16 And the R proteins may be receptors.
00:05:59;13 They may be in the membrane of the plant cell.
00:06:01;20 So, it indicated this classical ligand-receptor kind of interaction.
00:06:08;16 When the Avr genes and R genes are cloned,
00:06:12;23 you know, we'll see whether this model actually holds, right?
00:06:15;16 So, as I said, many R genes have been cloned from different species
00:06:20;20 against different kinds of pathogens.
00:06:21;29 So, we have N gene cloned from tobacco
00:06:24;03 against a viral pathogen.
00:06:25;25 A Cf9 gene... you know, the names... it's not important...
00:06:30;01 but this particular gene is against a fungal disease called leaf mold.
00:06:35;00 There's also, you know, genes...
00:06:37;19 R genes that are against bacterial diseases,
00:06:40;25 in this case, from Arabidopsis.
00:06:42;22 And also some R genes actually
00:06:45;16 against worms, like, nematodes.
00:06:48;20 So, it's very different kinds of pathogens.
00:06:52;06 Initially, we were thinking that maybe there's different kind of R genes,
00:06:53;26 you know, molecularly.
00:06:55;10 But it turns out many of these genes actually share the same kind of motif,
00:06:58;15 including the so-called leucine-rich repeat, or LRR.
00:07:02;25 And this is very exciting because
00:07:04;25 if you line up a sequence against a database,
00:07:07;01 some of the genes that come up are actually
00:07:10;03 involved in animal immune... immunity, so immune receptors,
00:07:13;09 for instance Nod1 is the bottom one diagrammed here.
00:07:17;04 It contains the leucine-rich repeat
00:07:19;24 like the plant receptors here.
00:07:21;06 It also contains so-called NB domains,
00:07:23;13 or nucleotide binding domains.
00:07:25;19 So, here's a very interesting parallel
00:07:27;23 between the animal immune system and the plant immune system.
00:07:31;00 They are based on the same kind of protein
00:07:35;02 to defend against different kinds of pathogens.
00:07:37;06 So, remember this model that I showed you just a few minutes earlier,
00:07:40;22 that indicated that these Avr proteins
00:07:43;16 may be secreted from the pathogen
00:07:45;29 and the R proteins are probably localized
00:07:48;19 to the plasma membrane in the host cell.
00:07:51;11 When you look at the Avr protein sequence, however,
00:07:54;14 you actually don't see this classical signal peptide
00:07:56;20 that indicates the protein will be secreted
00:07:59;02 through the conventional secretion system in the bacteria.
00:08:04;27 So, this model is probably not correct
00:08:07;02 in terms of this particular step.
00:08:09;06 Actually, it turns out most R proteins
00:08:12;09 are also not localized to the plant plasma membrane as originally predicted.
00:08:16;05 Most of them actually localize inside of the cytosol.
00:08:19;27 So, what's going on?
00:08:21;24 Now, this is really Puzzle #1 for a lot of people.
00:08:24;13 It doesn't really make sense.
00:08:26;17 Until we discovered that, actually,
00:08:29;14 most of these Avr proteins from bacteria
00:08:32;12 actually are directly injected into the plant cell
00:08:35;07 through the type III secretion system.
00:08:38;16 And this is actually a very conserved system
00:08:41;04 in bacterial pathogens of plants and animals, again.
00:08:45;02 So, you can see that type III secretion system.
00:08:49;10 You can see it under the electron microscope
00:08:51;24 like a syringe-like thing.
00:08:54;15 The injection system allows bacteria, in this case,
00:08:57;29 to penetrate through the plant cell wall.
00:09:00;22 So, the plant cell has a cell wall, unlike the animal cell.
00:09:04;03 And injecting through the plasma membrane into the cytosol.
00:09:07;07 So, that explains why Avr proteins
00:09:09;20 could be potentially recognized by R proteins
00:09:12;06 located inside the plant cell.
00:09:15;25 And this translocation system actually
00:09:18;14 is very common for other types of plant pathogen:
00:09:21;00 fungus and even, you know, nematodes.
00:09:24;14 They inject these proteins into the plant cell
00:09:28;04 as a very common mechanism during infection.
00:09:31;03 So, gene-for-gene resistance, you know,
00:09:33;24 became effector-triggered immunity, the common term today.
00:09:36;15 This is another way of depicting it.
00:09:38;04 So, you can see that bacteria
00:09:40;12 are injecting these red colored effectors
00:09:43;06 into the plant cell.
00:09:44;25 And they're being recognized by these immune receptors,
00:09:48;16 either containing the coiled-coil domain, CC domain,
00:09:51;16 or the TIR domain, and they are LRR proteins.
00:09:55;28 Okay? So, it's called effector-triggered immunity.
00:09:58;16 So, when the plant genome was sequenced in early 2000,
00:10:03;22 first from Arabidopsis,
00:10:05;08 people were interested to see how many R proteins are there in plants, right?
00:10:09;18 In humans, we know we have these antibodies.
00:10:11;26 You know, it's this endless combination of antibodies
00:10:15;13 that can recognize all kinds of microbes, right?,
00:10:18;00 10^14 specificity.
00:10:20;23 So, we wanted to know how many R proteins
00:10:23;02 are encoded from the plant genome.
00:10:25;15 There was a puzzle, actually.
00:10:27;05 When you see this, there's only hundreds of these genes.
00:10:30;05 How can hundreds of genes, immune receptors,
00:10:32;13 recognize thousands of microbes?
00:10:34;10 So, that's really a big puzzle.
00:10:35;21 And that was the puzzle based on this directed recognition,
00:10:38;20 so, saying that one Avr protein from a pathogen
00:10:42;15 can be recognized by a particular R protein in the plant.
00:10:46;20 So, it can't do this more than a hundred times, right?
00:10:49;19 This puzzle was partially solved by this realization
00:10:53;19 that there's a lot of so-called indirect recognition
00:10:57;00 by R proteins of these Avr proteins.
00:11:00;16 So, this is actually happening in many diseases.
00:11:03;19 So, this is a one example.
00:11:05;19 Imagine that this light blue colored circle
00:11:09;20 is a plant protein called RIN4 in Arabidopsis.
00:11:12;09 This protein is actually attacked
00:11:14;21 by two avirulence proteins, AvrB and AvrRpm1
00:11:18;05 from Pseudomonas syringae.
00:11:19;24 What they do is that these two Avr proteins,
00:11:22;20 well, they attack a RIN4 protein,
00:11:25;09 in this case inducing the phosphorylation of RIN4,
00:11:28;00 of the plant protein.
00:11:29;24 This phosphorylation event induced by two different Avr proteins
00:11:34;08 is recognized by the Rpm1 R protein.
00:11:37;08 Okay, so in this case one R protein recognized
00:11:41;02 two Avr proteins through this common modification
00:11:44;05 of another plant protein.
00:11:46;00 It's called indirect recognition.
00:11:47;29 There's actually another Avr protein called AvrRpt2,
00:11:50;22 which modifies RIN4 differently.
00:11:53;05 It actually cleaves the RIN4 because it's a protease.
00:11:56;02 That is being recognized by another R protein called Rps2.
00:12:00;10 So, you can see there's a lot of variations of so-called indirect recognition
00:12:03;15 that could potentially explain why a limited set of R proteins
00:12:07;20 could potentially recognize many different Avr proteins
00:12:10;29 from different pathogens, because they could induce modification
00:12:15;10 of another plant protein and that modification, then,
00:12:18;11 is sensed by the pathogen to say, this is not normal;
00:12:20;24 it's not my normal thing, okay?
00:12:23;12 So... so then there's another puzzle, okay?
00:12:25;13 I've being telling you these avirulence proteins from pathogens...
00:12:30;01 indicating... when you have these Avr proteins,
00:12:33;02 then the pathogen is avirulent. Okay?
00:12:35;17 Why would a pathogen send avirulence proteins
00:12:37;29 into the plant cell to become avirulent?
00:12:40;01 That... no... no... that makes no sense, okay?
00:12:42;25 And so that's Puzzle #3.
00:12:44;18 Why would the pathogen send avirulence proteins
00:12:46;27 into the plant to be recognized by R proteins?
00:12:49;13 What is the original function of these proteins? Okay?
00:12:52;18 So, I'll remind you of this again.
00:12:54;25 So, we have been talking about this effector-triggered immunity
00:12:57;10 because these particular cells contain R proteins.
00:13:01;16 The plants are resistant against pathogens, okay?
00:13:04;06 In this case, the effector proteins, or avirulence proteins,
00:13:08;07 are basically not good for pathogens.
00:13:11;02 They're being recognized.
00:13:13;04 Actually, in most plants without resistant proteins,
00:13:16;25 these effector proteins or avirulence proteins are doing something else.
00:13:20;12 They're actually suppressing another branch of immune response
00:13:23;28 called pattern-triggered immunity.
00:13:26;00 So, this is depicted on the left.
00:13:28;04 So, pattern-triggered immunity is distinct
00:13:30;13 from effector-triggered immunity.
00:13:32;07 They use different signaling pathways.
00:13:34;28 But they are normally suppressed
00:13:37;09 by these effector proteins to induce disease, okay?
00:13:41;00 So, that's why you want to send these Avr proteins into the plant cells,
00:13:44;13 because the R protein is rare.
00:13:48;01 So, what is pattern-triggered immunity?
00:13:51;03 This branch of immunity is not triggered by effectors
00:13:54;14 of the pathogen,
00:13:55;28 but it's triggered by common patterns from microbes.
00:13:59;13 There can be pathogens.
00:14:01;09 It could be non-pathogens, okay?
00:14:03;17 And so, they've evolved to recognize all kinds of microbes.
00:14:06;25 They are probably more ancient then effector-triggered immunity.
00:14:10;03 They are probably more related to the animal system of the immune system.
00:14:15;02 So, one example of these patterns from bacteria is called bacterial flagellin.
00:14:19;25 This is obviously very common
00:14:21;24 because most bacteria have to swim,
00:14:23;14 so they have to have these traits.
00:14:25;12 And that common trait is now recognized by pattern-triggered immunity.
00:14:29;02 So, one example you can see here...
00:14:32;04 you know, flagellin subunits make up the flagella.
00:14:35;12 It's like about 10,000 copies of this to make
00:14:38;26 a viable flagella.
00:14:40;13 Flagellin has a conserved domain at the N-terminus and the C-terminus,
00:14:43;21 a variable region in the middle of the protein,
00:14:46;28 and there's a peptide called flg22.
00:14:50;27 This is a 22- amino acid peptide,
00:14:54;02 which is now used very commonly in the study of
00:14:57;00 pattern-triggered immunity, called flg22.
00:14:59;03 People have identified the receptor in Arabidopsis for flg22
00:15:04;03 and flagellin.
00:15:06;06 This is done by Thomas Boller's group, very nice work.
00:15:09;15 This receptor looks like a traditional membrane-bound receptor.
00:15:14;14 You have a leucine-rich repeat domain,
00:15:16;27 which recognizes the flagellin or flg22 peptide,
00:15:19;27 but then you have a kinase domain inside the plant cell
00:15:22;25 that transduces the signal to do phosphorylation.
00:15:25;16 So, it's very similar to the animal signal/receptor system.
00:15:29;24 A critical question is,
00:15:32;09 is this receptor important for disease resistance, right? Okay.
00:15:36;14 So, this is done by Cyril Zipfel in Thomas Boller's group,
00:15:42;00 many years ago now.
00:15:44;05 They created this receptor mutant in Arabidopsis.
00:15:47;22 So, this mutant will fail to recognize flagellin of bacteria,
00:15:51;08 including Pseudomonas syringae.
00:15:52;29 On the left, you have a wild type plant
00:15:55;22 containing the full, functional fls2 receptor.
00:15:57;20 On the right is the receptor mutant.
00:16:01;20 And you can see... you see more disease after infection with Pseudomonas
00:16:06;02 in the receptor mutant compared to the wild type,
00:16:07;29 indicating the receptor is very important.
00:16:10;18 The importance of the receptor is actually most obvious
00:16:13;07 if the infection is done by putting bacteria
00:16:15;24 onto the leaf surface, okay?
00:16:18;03 For bacteria to infect the plants,
00:16:20;06 bacteria have to actually go into the leaves.
00:16:22;10 And one of the routes is through stomata.
00:16:25;08 So, these are microscopic pores on plant leaves
00:16:29;10 that allow plants to uptake CO2 to do photosynthesis.
00:16:32;25 But the stomata pores are big enough for bacteria to go in there,
00:16:36;29 so for a long time people thought this is a passive process.
00:16:40;24 The bacteria takes advantage of the open pores
00:16:43;00 to get into the plant tissue.
00:16:46;12 But I just told you...
00:16:48;16 so, the fls2 receptor mutant phenotype
00:16:52;21 is most obvious when you inoculate bacteria
00:16:55;16 onto the surface because they have to go through the stomata to infect.
00:16:59;17 If you inject bacteria directly into the leaf,
00:17:04;02 bypassing the stomata,
00:17:06;08 there's not much difference between the wild type plants
00:17:08;25 and the immune receptor mutant plants.
00:17:10;25 Okay, so, why?
00:17:12;20 It turns out... actually, my group figured out...
00:17:15;16 that this is because...
00:17:18;17 these are stomata cells that...
00:17:20;22 each stomata is actually made up of two guard cells.
00:17:23;02 They actually can recognize flagellin as a molecular pattern
00:17:26;28 and then they close the pore.
00:17:29;08 It's the first line of defense against bacterial infection.
00:17:32;09 So, this is a kind of interesting immune output,
00:17:35;14 very unique to plants.
00:17:37;21 They're recognizing the molecular pattern
00:17:39;24 and do this stomata closure as the first line of defense.
00:17:45;01 So, to summarize this part of the talk,
00:17:48;03 there are two branches of plant innate immune systems.
00:17:53;14 One is involving pattern-triggered immunity,
00:17:55;24 probably very ancient.
00:17:57;16 It evolved to recognize all kinds of pathogens or non-pathogens
00:18:02;05 so the plants won't be eaten by these microbes, then,
00:18:06;05 because plants are really rich in sugars and other nutrients.
00:18:10;18 But then, the pathogen has evolved effectors
00:18:14;02 to shut down the pattern-triggered immunity
00:18:16;09 as a mechanism of pathogenesis.
00:18:18;08 And this is a called effector-trigger susceptibility.
00:18:22;24 But then plants are smart.
00:18:25;11 They evolved this effector-triggered immunity to recognize individual effectors,
00:18:29;02 which used to be called avirulence proteins,
00:18:31;24 to activate the second branch of immunity
00:18:34;20 to fight against these pathogens.
00:18:37;01 So, this... if you go into the wheat field right now,
00:18:40;09 you have this continuation of evolution.
00:18:43;01 Sometimes the pathogen wins; sometimes the plants win.
00:18:45;24 What we want to do is to identify a way
00:18:48;23 to speed up the evolution so that we can fight against plant...
00:18:53;12 emergence of new diseases before they become a problem.
00:18:57;01 So, now I want to acknowledge colleagues
00:19:00;14 who actually gave me some slides for this talk,
00:19:02;06 so, including the slides I had,
00:19:04;13 Cyril Zipfel provided a few interesting slides for this part of my talk.
00:19:08;01 Thank you very much.

Part 2: Arabidopsis thaliana-Pseudomonas syringae interaction: The effect of climate in plant disease

00:00:07;22 Hello.
00:00:08;22 I'm Sheng Yang He.
00:00:09;23 I am a professor at Michigan State University and an Investigator at the Howard Hughes Medical Institute.
00:00:15;24 This is Part 2 of my iBiology talk.
00:00:19;08 In this part of my talk, I want to tell you some of our work involving Arabidopsis and
00:00:27;06 the Pseudomonas syringae interactions.
00:00:29;06 Particularly, I want to highlight one aspect of our research, illustrating how environmental conditions
00:00:34;24 could profoundly influence disease development in plants.
00:00:39;21 So, as you know, when you look at a plant growing in nature, outside, they not only are,
00:00:47;07 you know, exposed to potential pathogens, but they are also experiencing a lot of different conditions:
00:00:52;24 temperature fluctuation, you know, from morning to evenings; light, as you can see here;
00:00:59;20 and temperature; humidity; and microbiome, even.
00:01:03;23 We know that all of these factors actually influence pathogen and plant interactions.
00:01:09;09 The molecular bases of this are not well understood.
00:01:12;24 And so some famous scientist said, you know, without understanding environmental conditions,
00:01:16;26 we will never understand the immunity in plants... you know, in the plant system.
00:01:23;04 So, I'll just give you a couple of examples of how important the climate conditions could be
00:01:28;00 for plant disease outbreak in the field.
00:01:32;11 This is the bacterial fire blight disease in apple.
00:01:36;11 This is in Switzerland.
00:01:37;11 This is a 12-year span of disease incidents from 1995 to 2007.
00:01:45;18 So, apples are always growing in, you know, Switzerland, and pathogens are always in these orchards,
00:01:50;20 but you don't see the disease every year.
00:01:53;15 And the reason is for disease to occur you need a lot of humidity and the right temperature, right?
00:02:01;10 So, in 2007, in that year you have heavy rain and high humidity in the spring,
00:02:05;23 when the apple was flowering, and these bacteria tend to infect the flowering parts.
00:02:11;19 And so everything kind of came at the same time, and then have very severe disease.
00:02:16;17 So, that's one example.
00:02:19;08 Another example is called fusarium head blight of wheat.
00:02:23;07 This is actually a very huge global disease right now.
00:02:28;11 It's also favored by high humidity and warm temperatures in the spring.
00:02:31;22 So, you can see that... you know, normally you see a nice green top of the wheat.
00:02:38;03 In this image, you can see, basically, bleached grains.
00:02:43;15 And there were four very severe epidemics in China in the last five years,
00:02:47;28 so almost every year has very severe disease.
00:02:49;25 This disease, also, is very serious, because the fungus actually produces a toxin
00:02:56;11 which makes us sick.
00:02:57;11 And so... not only reducing yield, but also causing sickness in the human population.
00:03:05;15 So, I want to tell you that plant diseases are really, you know, problems in modern agriculture.
00:03:11;19 They're really major threats to food security, globally, right now.
00:03:16;19 Some of these diseases are very old.
00:03:18;28 On the left is a disease called rice blast, a disease I actually grew up, when in China
00:03:25;04 I lived in a village with 200 people or so.
00:03:29;04 So, you know, I saw this rice blast when I was a really small little child.
00:03:35;01 When I go back right now, 40 years later, and talk to my parents, and this is
00:03:41;04 still the number one disease locally, but also globally, in rice production.
00:03:45;06 So, many old diseases continue to really pose major problems.
00:03:49;10 Now, you also have new diseases coming up.
00:03:52;20 One example I'm giving to you here is a kiwi bacterial canker, which is caused by
00:03:57;14 a bacterial pathogen called Pseudomonas syringae, and I'm going to tell you a little bit about that today.
00:04:02;12 So, this is despite all the chemical input -- you know, pesticides, you have to spray them,
00:04:08;09 farms have to use them, because otherwise you won't have, you know, really high yield --
00:04:11;20 but also all the breeding efforts, that many scientists try to breed resistant cultivars.
00:04:18;21 You know, from wheat to rice, based on these so-called disease resistant genes.
00:04:25;03 But this is not enough.
00:04:26;03 So... because we have disease every year still.
00:04:28;18 One of the problems, as we've realized, is that we really don't understand
00:04:32;05 the basic process of disease, okay?
00:04:34;16 So, this is an area that we really want to push ahead.
00:04:39;02 So, in the last 15 years or so, you know, many laboratories including us are
00:04:45;11 really concentrating on trying to work out why disease occurs.
00:04:49;22 And so this is an overview of different kind of pathogens that can cause disease in plants.
00:04:54;19 So, we have fungus; we have bacteria; we have nematode, worms, you know; and viruses.
00:05:03;02 Many of these pathogens also cause problems in our human bodies also.
00:05:06;25 And so one... so, they look very different, but one of the common things they do is to
00:05:10;18 deliver these virulence factors -- collectively, we call them effectors -- into the plant cell.
00:05:16;27 And... and so, they use different ways of delivering these virulence proteins.
00:05:21;20 In the case of bacteria, they use a secretion system called the type III secretion system.
00:05:26;02 You can see on the right a syringe-like structure, here.
00:05:31;08 If you knock out this delivery system, bacteria become non-pathogenic, okay?
00:05:35;22 So, that illustrates how important these virulence factors are to causing diseases.
00:05:41;06 So, because of that, studying how effectors work really can provide great progress into
00:05:48;25 the molecular basis of disease susceptibility.
00:05:52;27 And interestingly, these molecules, microbial molecules, also can be very powerful probes
00:05:58;19 into the fundamental biology of the host -- and that can be plants or it could be humans --
00:06:03;13 because they usually find very intriguing RNAs or proteins or DNAs to manipulate the host physiology.
00:06:09;27 Okay, so in a sense, this is a really great, you know, probe into the biology of the host itself.
00:06:16;08 Obviously, discovering the target of these virulence factors could offer new leads into
00:06:21;24 innovative disease control we really desperately need right now.
00:06:25;25 So, how do we understand disease susceptibility?
00:06:28;07 Which approaches?
00:06:29;23 We and others are really following this very simple diagram, here.
00:06:32;24 We want to understand the host target of all these bacterial virulence proteins.
00:06:38;17 So, in the case of the bacteria we study, it has about, you know, 30 or so effectors.
00:06:43;04 What we want to do -- we means us and the many other laboratories -- is really to identify
00:06:48;12 these host proteins or RNAs or DNAs that are being targeted by these virulence factors,
00:06:54;12 and we want to associate these host targets to these particular pathways.
00:06:58;05 You know, I listed the five of them -- A, B, C, D, E -- but it could be 30, right?
00:07:02;28 So, we don't know how many pathways are being targeted by bacterial virulence factors.
00:07:08;00 What we hope to do is to... once we identify these pathways, we could genetically
00:07:14;00 perturb these pathways in the host, in this case, in the plant.
00:07:17;25 And if we're successful, then if we understood everything about the disease process,
00:07:23;13 we can create a poly mutant of the host in which these pathways are basically either
00:07:29;16 activated or inactivated to simulate the collective activity of these virulence factors.
00:07:36;03 And then if we really understood the process then, then the poly mutant of the host
00:07:40;05 would be susceptible to a bacteria that is not able to produce effectors.
00:07:44;22 In other words, if we manipulate the host already, genetically, to simulate the
00:07:50;17 action of the virulence factors, you don't need these virulence factors to start with, right?
00:07:53;28 Until then, we will never know we understood the disease, okay?
00:07:56;27 So, that's the goal.
00:07:58;06 It's very challenging, but by the end of these twenty minutes, I want to show you that
00:08:02;05 we have made progress towards that goal.
00:08:04;28 So, we use this very simple model system involving Arabidopsis, which is a model plant,
00:08:12;04 and a bacterial pathogen called Pseudomonas syringae.
00:08:14;21 It's a very common pathogen.
00:08:16;13 It infects virtually all crop plants in the field, okay?
00:08:20;25 Each individual string of this species, Pseudomonas syringae, infects a very narrow range of hosts.
00:08:27;02 So for instance, strain DC3000 in the field only infects tomato.
00:08:32;24 In the laboratory, you can also make it infect Arabidopsis, okay?
00:08:37;05 So... so because Arabidopsis is a very, you know, powerful model for plant research...
00:08:42;05 so we have been working on Arabidopsis-Pseudomonas model system for many years now.
00:08:48;00 Pseudomonas can actually live on the surface of the bacteria... of the plants as an epiphyte.
00:08:54;15 But in order to cause disease, it has to go into the interior of the leaf, in this case, okay?
00:09:00;20 They go into the leaves through so-called stomata.
00:09:03;16 So, these are microscopic pores on the leaf epidermis that allow plants to take up
00:09:09;15 the CO2 to make food for us, okay?
00:09:12;02 So, photosynthesis.
00:09:13;02 It's very important, okay?
00:09:15;22 And once bacteria go into the... inside the leaf, it lives in between the cells, okay?
00:09:21;09 So, these are called mesophyll cells.
00:09:23;12 So, these are extracellular pathogens, okay?
00:09:25;21 So, this space is called the apoplast.
00:09:27;06 Now, I want to tell you the apoplast is normally filled with air.
00:09:31;13 It's not filled with liquid.
00:09:32;13 This is very important, because CO2 has to go into the... goes through to the stomata
00:09:37;18 into the apoplast, but it has to diffuse into the mesophyll cell and the chloroplast.
00:09:42;04 So, it's a long distance for the CO2 to go in there.
00:09:45;03 You don't want water in there, because there will be very high resistance to CO2.
00:09:51;00 So, the plant has a way of keeping that space mostly filled with air.
00:09:55;04 I'll come back to this.
00:09:56;04 It's actually very relevant to pathogenesis.
00:09:58;22 So, what we do in the laboratory to kind of have a disease assay is really to grow plants
00:10:04;08 in a pot.
00:10:05;25 You probably do this at home.
00:10:07;14 Not this style, but in another way.
00:10:10;01 And then, when they are four or five weeks old, we would dip the plants entirely
00:10:15;19 into the bacterial suspension and wait for, basically, three days, okay?
00:10:19;11 You will see disease symptoms, as shown here.
00:10:21;15 So, I'm gonna play a movie which shows you the time-lapse video of the infection process.
00:10:28;05 On the left are the mock...
00:10:29;19 I mean, are the bacterially infected plants.
00:10:33;04 On the right is a mock infection, this is water, okay?
00:10:35;24 So, what you can see, now... eventually, you can see the yellowing on the plants that are infected.
00:10:42;00 And on the right are the ones that are moving, you know, they are alive, okay?
00:10:45;17 You can see there are some plants that are kind of dancing, of this thing you can see.
00:10:50;12 But the infected plants are basically paralyzed, okay?
00:10:53;02 So, we actually don't know why plants are motionless very early on in the disease.
00:10:58;00 This is one of the things we are trying to understand in the... in the next few years.
00:11:02;18 So, we have worked on several aspects of this disease process.
00:11:08;14 For instance, we have, a few years ago, figured out that entry process, right?, how bacteria
00:11:15;07 enter the plant tissues through the stomata.
00:11:18;25 For a long time, scientists think they are passive, because the stomata pores are
00:11:24;11 quite big and bacteria are kind of small.
00:11:25;26 They can... the pore has to be open for photosynthesis during the day, so we always thought bacteria
00:11:31;11 can just take advantage of that and go into the tissue, like, passively, right?
00:11:34;17 That doesn't turn out to be the case.
00:11:37;00 It turns out these guard cells -- there are two guard cells to form one stomata pore --
00:11:42;18 they actually can sense bacteria.
00:11:45;03 And so once they sense the bacteria, they close it as the first line of defense,
00:11:50;02 to prevent any microbes entering the tissue.
00:11:52;27 So, plants are very smart, okay?
00:11:54;12 So, that's about... a very intriguing mechanism defending against pathogen invasion.
00:12:00;23 We discovered one of the... so, that's bad for the bacterial pathogen, right?
00:12:04;00 It cannot even start the infection.
00:12:05;12 So, in the case of Pseudomonas syringae, it figured out a way to prevent that from happening
00:12:10;02 by producing a toxin called coronatine, which prevents stomata from closing.
00:12:15;07 And so the bacteria can massively infect to start an infection.
00:12:20;14 Once the bacteria get into the mesophyll space... as I mentioned before, it's an extracellular pathogen,
00:12:25;13 but it makes a type III secretion system injecting more virulence effectors
00:12:30;01 into the plant cell as a major weapon of pathogenesis.
00:12:32;28 So, we're working on this area as well.
00:12:35;28 So, we knew a little bit of these basic steps of this infection involving stomata entry,
00:12:41;13 involving a toxin that prevents the stomata from closing, and involving these effectors
00:12:46;17 that we think, now, are suppressing immune responses in plants, okay?
00:12:51;07 Work in the past few years, from us and many other groups, has deepened our understanding
00:12:56;26 of these basic steps, but also... in our case, we realized that we're missing two dimensions
00:13:02;21 in the last, you know, many years, actually.
00:13:05;00 One dimension involves the profound effect of environmental conditions on the host-pathogen interactions.
00:13:10;19 So, that's under the left circle, here.
00:13:14;13 We also started to realize the endogenous microbiome -- the plant also has a microbiome --
00:13:19;00 has tremendous effect on host-pathogen interactions.
00:13:21;21 So, these are new directions.
00:13:22;27 I'm gonna highlight one particular area, which is involving how environmental conditions
00:13:28;17 could influence the disease interactions, okay?
00:13:31;24 So, we are focusing on two areas.
00:13:34;27 One is the temperature, how elevated temperatures could influence disease.
00:13:39;09 This is actually very relevant right now with climate change.
00:13:42;16 The globe is warming.
00:13:44;11 But also, more importantly, the heat waves we're experiencing in different countries
00:13:49;06 are very severe right now... and how these short periods of heat waves could influence infection.
00:13:55;26 Okay, so this is one of my students, Bethany Huot, who recently published a paper
00:14:00;20 just showing very simply... you can see under... we grow plants the same way, okay?,
00:14:05;15 but during infection we put the plants in 23 degrees, which is the normal temperature, or you shift
00:14:11;04 5 degrees up, to 28 degrees, you can see dramatic differences already.
00:14:15;08 At the warm temperature, you see much more severe disease, okay?
00:14:19;20 She discovered this is based on two mechanisms.
00:14:22;21 One is the warm temperature actually enhances greatly the virulence expression.
00:14:26;28 So, the effector secretion into the plants is greatly enhanced.
00:14:32;05 But also, she discovered that the immune signaling in the host is completely shut down.
00:14:37;21 So, this is actually very important in the field, you know.
00:14:40;21 The immune pathway that she was working on is called salicylic acid signaling,
00:14:45;28 which is mimicking, like, the aspirin we take sometimes.
00:14:48;00 It's a similar chemical.
00:14:49;14 It boosts the immune response.
00:14:51;17 This response is shut down by warm temperature.
00:14:54;15 This could have a profound influence in the field, crop resistance, because most of the
00:14:58;28 crop resistance is based on their signaling cascades.
00:15:01;12 So, we don't know the details of this pathway.
00:15:03;24 This is something we're gonna work out in the next few years.
00:15:05;24 What I'm going to talk to you about in more detail is humidity's effect on plant disease,
00:15:11;02 okay?
00:15:12;02 This became, actually, obvious in our disease reconstitution experiment I mentioned in the
00:15:15;12 beginning of my talk.
00:15:16;21 We tried to figure out how many pathways are being manipulated by the bacterial pathogen.
00:15:21;18 And ultimately, we want to create a poly mutant of the plant to see whether we can
00:15:26;21 rescue the pathogenesis of a bacteria that does not, you know, deliver any of these effectors,
00:15:31;12 okay?
00:15:32;12 So, that's a very daunting task, but we... as scientists, we want to, you know,
00:15:37;08 face the challenge and try to work it out.
00:15:39;22 So, there are 30 of so effectors, I told you, in this particular bacterium, so we and others
00:15:45;03 are systematically going through to identify the host target of each of these effectors,
00:15:49;16 okay?
00:15:50;16 A model that we and others have developed in the last, you know, 15 years or so about
00:15:55;25 the function of these effectors is this, in a simple way.
00:15:58;27 So, you're seeing a bacteria sitting on the plant cell wall.
00:16:02;10 So, a plant cell, unlike an animal cell, has a cell wall surrounding it.
00:16:05;18 But in the plasma membrane, which you can see, there are receptors.
00:16:09;17 They're called immune receptors, that perceive these patterns from microbes, in this case,
00:16:14;16 flagella, these wavy things, very common for bacteria.
00:16:18;07 And once they sense these molecules, it then triggers a signal transduction pathway
00:16:22;20 -- this is a very simple diagram -- eventually leading to a form of immunity called pattern-triggered immunity.
00:16:29;06 So, this is bad for bacteria, so what bacteria are doing is to send these effectors
00:16:34;06 into the plant cell to attack different steps of this signaling cascade, to shut down
00:16:38;24 this form of immunity.
00:16:39;24 It's a major mechanism of disease.
00:16:43;05 And so, I'll just give you one example from a collaborative work from Cyril Zipfel's group
00:16:48;11 and my laboratory, also, involving a particular effector called HopAO1.
00:16:53;01 HopAO1 biochemically is a phosphatase, which removes phosphate from proteins.
00:16:59;22 And it turns out these immune receptors are phosphorylated, normally, during activation
00:17:04;14 at a tyrosine residue of the protein.
00:17:07;11 And this effector actually removes the phosphate from tyrosine to shut down this immune activation.
00:17:12;02 So, this is a very cute way of... you know, bacteria figured out how to kind of sabotage
00:17:17;14 the immune signaling.
00:17:18;18 And there are many studies to support this, very strong evidence that this is really true.
00:17:23;10 So, one of the major functions of these virulence factors is to shut down the plant immune response, right?
00:17:29;10 If there's no immunity response in the host then you can, you know, infect the plants.
00:17:32;16 And this is very similar to human pathogenesis.
00:17:35;03 And many of the bacterial pathogens are human pathogens that actually do the same thing.
00:17:39;02 They're shutting down the immune system in our body, then infect.
00:17:42;22 Okay, so our question is this.
00:17:44;20 Are all these 30 or so effectors involved in immune suppression?
00:17:48;06 If they're all attacking, you know, immune suppression, then we can reconstitute the disease
00:17:53;23 by using the immune compromised plants, right?
00:17:56;27 So, I'm coming back to point... that point later.
00:17:59;13 I've introduced you to two bacterial strains, now.
00:18:02;10 I'm talking about the wild type strain, DC3000.
00:18:05;17 It secretes these 30 or so effectors into the plant cell.
00:18:08;13 There's a mutant called delta-28E, which has 28 of these 30 effectors deleted.
00:18:14;27 It has involved a lot of work done by Alan Collmer's lab at Cornell University,
00:18:21;02 but they did it, so it's a very useful mutant, and we take advantage of this mutant.
00:18:25;20 Because this mutant has essentially no effectors that are delivered into the plant cell,
00:18:30;04 it's not pathogenic.
00:18:31;04 So, if you put into a wild type plant... you can see that on the left is infection by DC3000.
00:18:36;12 It causes disease-like symptoms.
00:18:38;09 But on the right is green; it's a healthy plant.
00:18:40;28 So, this mutant cannot cause disease in the wild type plants.
00:18:45;22 If, as I said, all effectors are attacking the immune signaling, then if we start with
00:18:51;22 immune defective plants, if there's no immunity in the plants, then this mutant, delta-28E,
00:18:58;27 should be able to infect the plants, right?
00:19:01;22 Okay, so that's the experiment we did.
00:19:03;23 You can see that, unfortunately, the delta-28E mutant was unable to cause disease.
00:19:09;14 You know, the plants are still kind of green after infection, okay?
00:19:13;04 The mutants we used, fec and bbc, these are defective immune responses in the plants.
00:19:18;16 So, the answer is no.
00:19:19;28 Okay?
00:19:20;28 So, you can also look at the bacterial population.
00:19:22;21 So, when the plants are infected by Pseudomonas syringae, it multiplied really high.
00:19:27;17 So, this is... the bar is in the logarithm... log-type scale, so each step is a tenfold increase.
00:19:36;04 You can see that DC3000 aggressively multiplied inside the leaf.
00:19:40;20 Versus the delta-28E in wild type and in mutant leaves, they are unable to achieve
00:19:47;10 a very high population.
00:19:48;10 So, there's no disease, so the answer is no.
00:19:50;05 So, the question is, what are we missing?, right?
00:19:52;26 So, some effectors must be attacking something other than immunity as a part of their mechanism.
00:19:59;02 So, I'm gonna pull you away from my... our own results to tell you something about a website.
00:20:05;22 So, if you're growing plants in your garden, this is actually for master gardeners,
00:20:10;09 so anything written on this website must be true because you have to follow that.
00:20:14;08 Okay, so you can see that I just took a few sentences out.
00:20:18;05 It says, bacterial diseases are most intense in warm and humid conditions like Florida,
00:20:23;26 okay?
00:20:24;26 So, Florida actually has a lot of diseases compared to California.
00:20:26;26 California is dry.
00:20:30;02 You can recapitulate... this is actually famous idea called the "disease triangle" dogma.
00:20:34;17 For a disease to occur, you not only need a planet which is susceptible genetically
00:20:38;06 and a pathogen which would is virulent genetically, but you also need a conducive environment.
00:20:42;26 One of the main factors is high humidity, okay, rains and things like that.
00:20:47;27 This was formulated by a very famous plant pathologist, RB Stevens, 50 years ago.
00:20:52;14 We actually don't know the molecular basis by which humidity is required for disease
00:20:56;03 very much.
00:20:58;08 You can recapitulate the humidity requirement in the laboratory.
00:21:01;07 Basically, you can grow plants, you know, for four weeks.
00:21:04;12 But during the infection period of three days, we either place the plants under high humidity,
00:21:09;13 like 95% percent, which simulates the disease outbreak condition in the field, or you,
00:21:15;02 you know, set up the plants at [30%], which is a low humidity.
00:21:19;20 You can see that at high... and only at high humidity you have disease.
00:21:22;16 At low humidity, plants look healthy.
00:21:25;11 And you can look at the disease bacterial population, also.
00:21:29;08 High humidity has a very high population, and under lower humidity you have very low.
00:21:34;20 Okay, so it's a dramatic difference, okay?
00:21:36;24 Now, if you go back to this website, you can also see a term called water soaking.
00:21:42;02 This is describing the symptom of the disease of many bacterial diseases.
00:21:45;24 Normally, if you look at leaves in your backyard you will see kind of, you know, green, okay?
00:21:51;15 There's no spots, right?
00:21:53;15 In this picture, you can see there's a lot of dark spots.
00:21:55;18 These dark spots are caused by liquid in the leaf.
00:22:00;17 And plants don't like that.
00:22:01;17 I just how you been beginning, for photosynthesis to occur, for CO2 to diffuse into the mesophyll cell,
00:22:06;10 you want to keep the apoplast air-filled.
00:22:09;20 And in these dark spots, there's liquid in there.
00:22:12;12 It's really bad for plants.
00:22:13;21 But bacteria seems to be able to do this for a purpose.
00:22:17;00 We are actually... so, phenomenon has been observed for many decades.
00:22:20;22 We don't know whether it's needed for pathogenesis, okay?
00:22:24;07 So, we were intrigued by this.
00:22:26;11 This only occurred under high humidity, also.
00:22:28;13 So, you can simulate this process in the laboratory.
00:22:31;24 This is our Arabidopsis, again, infected by Pseudomonas syringae.
00:22:36;10 You can see dark spots, here, on the right leaf, which is infected.
00:22:39;19 On the left, that was not infected.
00:22:41;25 This also occurred in tomato, because this bacteria also infected tomato.
00:22:45;01 So, under high humidity, you have this so-called water soaking symptom.
00:22:49;25 Now we can label bacteria to see where the bacteria are in the infected tissue by
00:22:55;18 loading it with a luc... you know, lucs emit light... allow bacteria to emit light.
00:23:00;28 So, you can catch the light emitted from bacteria in the infected tissue and then overlay this
00:23:07;25 with the water soaking symptom that you capture with regular light.
00:23:10;26 And if you see, in the bottom of the left leaf, we can see extensive overlap
00:23:16;18 between the luc -- the light indicating bacteria -- and the water soaking spots, suggesting that
00:23:24;17 the water soaked area is where bacteria multiply really highly, okay?
00:23:27;23 So, that is really spatially kind of indicating water soaking is quite important.
00:23:32;23 So, what causes the water soaking?
00:23:35;02 Okay, I told you this bacteria produces 30 or so effectors.
00:23:38;14 We actually screened each individual effector to see which one can cause water soaking.
00:23:43;14 In this experiment, we show that two of them can cause water soaking.
00:23:47;16 And the names are not very important, but I can show you that one is localized to
00:23:51;20 the plant plasma membrane, here.
00:23:54;01 One is localized to, actually, the endomembrane system in the plant cell, called the endosome,
00:23:58;26 which is involved in recycling all the proteins to and off the plasma membrane of the plant cell.
00:24:05;03 So, they're two... these two effectors are doing something to the plasma membrane
00:24:08;06 of the plant cell to cause water soaking.
00:24:11;24 We actually know a little bit more about one of these effectors.
00:24:14;01 They actually attack a protein in the plants that regulates the vesicle traffic.
00:24:19;02 So, it's a really intriguing phenomenon, also, because a lot of human pathogens also do that,
00:24:25;04 attack proteins that are involved in vesicle trafficking in our human cells as a way to
00:24:29;23 shutting down the immune system.
00:24:32;01 Okay.
00:24:33;01 So, now we have... in addition to the immune suppression process, we discovered a new process
00:24:38;14 we called aqueous apoplast, which is the inside of the leaf accumulating, basically,
00:24:43;17 water and other things.
00:24:45;11 Okay?
00:24:46;11 So, in order to cause water soaking, you need the so-called water soaking effectors
00:24:50;26 from bacteria.
00:24:51;26 But that's not sufficient.
00:24:52;26 You also need high humidity in the air.
00:24:55;23 The reason is that in the low humidity, even if the bacteria are producing water soaking symptoms,
00:25:01;05 it will be evaporated out through stomata, because stomata are open during the
00:25:04;24 day for... to take up CO2.
00:25:07;22 And because of that, if you have low humidity, the water just comes right out.
00:25:11;18 And because there's no water, then the bacteria will not benefit.
00:25:14;16 So, here's an example where we need variance factors in the bacteria and we need
00:25:18;18 the external environment to be humid, okay?
00:25:20;05 So, this is kind of interesting.
00:25:22;28 So now, the question.
00:25:23;28 The next question we want to ask is... okay, we have two processes now.
00:25:27;11 We know that immune suppression is not sufficient for pathogenesis.
00:25:31;00 Now we have two... are they sufficient, now, for pathogenesis?
00:25:35;00 So, this is a disease reconstitution experiment we always wanted to do.
00:25:39;15 So, we can simulate the suppression of the immune response in the plant by using
00:25:46;14 this mutant of Arabidopsis that is unable to mount an immune response.
00:25:50;00 We can also mimic the water accumulation in the apoplast by using this new mutant
00:25:55;06 that we have, called min7, okay?
00:25:57;08 The idea is to combine these two process by genetically manipulating the two pathways.
00:26:03;07 Using CRISPR/Cas9 technology, we created quadruple mutants, basically affecting both immunity
00:26:09;26 and water homeostasis.
00:26:11;27 So, the question is that, in these quadruple mutants, would bacteria that normally
00:26:17;25 cannot deliver any effectors... is going to multiply or not, okay?
00:26:22;02 So, this is the experiment we did.
00:26:24;09 So, the bacterial mutant we use is the bacteria that are unable to secrete any of these effectors,
00:26:28;25 that's defective in type III secretion, okay?
00:26:31;06 In the wild type plants, they don't cause disease.
00:26:34;06 It's green plants.
00:26:35;27 In these immune-defective mutants, it still does not cause disease, as I showed you before,
00:26:41;06 okay?
00:26:42;06 So, it's not sufficient.
00:26:43;13 In a min7 plant, also, it does not cause disease.
00:26:46;17 In the quadruple mutants, now, you can see disease-like symptoms.
00:26:50;11 And this is actually when we're seeing a non-pathogenic bacteria cause any disease on a plant system.
00:26:56;19 So this is pretty exciting to us.
00:26:58;24 If you look at the bacterial population in these leaves, you can see that the red bars
00:27:03;10 are indicating the quadruple mutants.
00:27:05;15 Only in these two quadruple mutants, you can start to see the multiplication of an otherwise
00:27:10;11 non-pathogenic bacteria, okay?
00:27:12;17 So, it's not to the extent of the totally wild type infection, so we have some distance to go,
00:27:16;08 but this is a quite significant step.
00:27:18;25 So, summarizing this part of my talk, we have identified a new pathogenic process involving
00:27:25;27 what we called aqueous living space.
00:27:29;04 We know bacteria loves water because, you know, human pathogens and plant pathogens
00:27:34;05 all love water, right?
00:27:35;13 So... but this is a case where bacteria actually create water conditions in an otherwise air-filled space.
00:27:43;22 And if you think about whether this is relevant to, you know, other diseases,
00:27:47;09 including human diseases like a lung infection and the respiratory system, which is normally filled with the air...
00:27:53;12 so, we will see whether this principle will go beyond plant diseases, okay?
00:27:57;17 We were able to reconstitute the basic features of a bacterial infection within
00:28:03;02 exclusively host mutants, okay?
00:28:05;03 So, that's also the first time we've done this.
00:28:08;02 Of course, we're getting some insight into why humidity could have profound influence
00:28:12;08 on the disease interactions.
00:28:15;13 In this case, because it's required for the virulence factors to function as virulence factors.
00:28:21;04 So now, I'd like to acknowledge the people that actually did the work.
00:28:24;07 Of course, my lab members at Michigan State.
00:28:28;01 And I also want to acknowledge a number of collaborators: Jeff Chang, Cyril Zipfel.
00:28:34;25 Also other investigators that I collaborated with for the other part of my talk.
00:28:40;24 Funding are from HHMI, Gordon and Betty Moore Foundation, NIH, DOE, USDA,
00:28:46;24 and the National Science Foundation.
00:28:49;02 Thank you.

Videos in this Talk

Part 1: Introduction to Plant-Pathogen Interactions
Audience:
- General Public
- Student
- Researcher
- Educators of H. School / Intro Undergrad
- Educators of Adv. Undergrad / Grad
Part 2: Arabidopsis thaliana-Pseudomonas syringae interaction: The effect of climate in plant disease
Audience:
- Student
- Researcher
- Educators of H. School / Intro Undergrad
- Educators of Adv. Undergrad / Grad

Speaker: Sheng-Yang He

Total Duration: 0:48:35

Recorded: December 2017

All Talks in Plant Biology

Talk Overview

What mechanisms do plants have to fight pathogens? In this seminar, Dr. Sheng-Yang He explores plant-pathogen interactions and provides an overview of a plant’s basic immunological responses. As He explains, plants have “resistant” genes, which trigger the immune response after pathogenic infections (effector-triggered immunity). Also, plants immune system can be activated by the recognition of general patterns in pathogens (pattern-triggered immunity). Understanding these interactions could aid in the prevention of disease in plants, which would be beneficial to the agricultural industry and global food security.

In his second lecture, He provides evidence on the effect of environmental factors (e.g. humidity) in the development of disease in plants. In order to understand disease susceptibility, his laboratory studies the interaction that Arabidopsis has with the bacteria Pseudomonas syringae. His laboratory showed that an increase in temperature and humidity increase bacterial disease severity. By genetically creating a plant that is altered in its immune system and water homeostasis, they were able to define the minimal factors that bacteria need to infect the plant.

Speaker Bio

Sheng-Yang He

Dr. Sheng-Yang He is a University Distinguished Professor at Michigan State University and a Howard Hughes Medical Institute investigator. He obtained his bachelor’s degree (1982) and a master’s degree in plant protection (1991) from Zhejiang Agricultural University in China. He pursued his graduate degree in plant pathology (1991) at Cornell University and continued his post-doctoral… Continue Reading