November 1, 2025 • 25 mins
How do plants defend themselves, fighting a war of attrition cell by cell? And how did a scientist in Minnesota in the 1950s reshape how we understand plant immune systems and the genetics at their heart. And of course, how does this all connect to GMOs? Let's find out.
References
- H. H. FLOR: PIONEER IN PHYTOPATHOLOGY
- Jin L, Chen M, Xiang M, Guo Z. RNAi-Based Antiviral Innate Immunity in Plants. Viruses. 2022 Feb 20;14(2):432.
- FAO. 2022. FAO’s Plant Production and Protection Division. Rome.
- PAPAYA RINGSPOT VIRUS (PRY): A SERIOUS DISEASE OF PAPAYA
- 2024 STATE AGRICULTURE OVERVIEW - Hawaii
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
The spores of the Flax Rust fungus keep very well in the refrigerator.
(00:04):
That's a mundane discovery that Harold Floor made as he went about his research, but
as so often in science, the mundane details can be what paves the way for major discoveries.
Harold Floor was an unassuming man.
A plant scientist working from the 1920s to the 1980s, he was born in St. Paul, Minnesota.
(00:25):
He loved hunting and fishing, and he didn't seem to care much for teaching or for mentoring
new students.
To be honest, from other things I've read about him, I can't say that I think Harold
and I would have had very much in common.
But there is at least one thing we had in common, a love of plant pathology.
Plant pathology is the study of plant diseases, plant immune systems, and had to protect crop
(00:45):
plants against diseases.
It is a field that Dr Floor dedicated his entire long career to, whereas I only dedicated
the five years of my PhD studies to it.
But this specific area of plant pathology that I worked on ultimately rests on Dr Floor's
discoveries, that is the study of plant pathogen effector proteins and the plant resistance
(01:06):
genes that defend against them.
Harold Floor's most impactful contribution wasn't so much any one factor finding though
he certainly made thousands and thousands of careful observations of fungal pathogens
of plant hosts, particularly the Flax plant and how they interact.
He would watch with practice patients as the tiny yellow proliferation of fungal mass would
(01:29):
grow at each infection site, spread across the leaf and eventually killed the leaf.
And he would watch just as closely with the help of a microscope how sometimes the spores
of the fungus would germinate, stretch out a hopeful, hyphil thread only to weather and
die, leaving a healthy leaf unbothered by the fungal threat.
And as he carefully tracked the results of these experiments over years, something started
(01:53):
to become clear to him.
He compared the results of these experiments to the conceptual models emerging in the 1930s
and 40s from the field of genetics, which by that point had grown over several decades
to become arguably the hottest field in life science.
Genetics had become a major part of the biological science mainstream and that had catalyzed
(02:13):
the explosion of plant breeding as we'll see in our next episode.
Harold Floor was not by any means the first person to try to use the tools of genetics
to understand plant diseases, and more specifically how some plants are able to resist disease
while others succumb.
It was already well established that there were genes that influence plant disease, resistance
(02:33):
and infection, with more resistant and less resistant alleles of these genes found.
It was already known that in most cases these genes were specific in their effect to certain
pathogen types.
And of course it was known that the pathogens themselves, whether they be bacteria, fungi
or viruses have their own genes and that certain pathogen genes affect how well they can
(02:56):
infect a host.
You may never have thought about it, but plants can be infected by the same sorts of organisms
as animals, including ourselves.
Though not generally the same species or strains, a virus that can infect plants won't be
able to infect animals and vice versa.
Fungai are much more of a problem for plants than they are for animals, with some of the most
(03:17):
devastating crop diseases caused by fungi.
Plants are also particularly plagued by the superficially fungus-like microorganisms called
"Umei seeds".
A famous example is Phytophthoro-infestans, the pathogen that caused potato crops to fail
in the 1840s in Ireland, which in the context of British colonial rule triggered a massive
(03:38):
and deadly famine.
There are some Umei seeds that infect humans, but overall Umei seeds are more of a plant
thing.
Plant tissues like animal tissues are stores of energy in biomolecules, a perfect food for
a hungry pathogen to feed on, grow and divide, and so microorganisms will try to invade and
(03:58):
get that energy and those nutrients.
We call that process an infection, and we call the organisms doing the infecting pathogens,
and that implies whether the infected host is a human or a hydrangea.
However, the particulars of plant biology do lead to some major differences when it comes
to thinking about how the experience and fight infections.
(04:20):
For instance, plant tissues are full of cellulose, and molecule that animals don't have.
Cellulose cell walls are both a major barrier in the way of pathogens, and a potential
source of energy for those able to break them down and digest them.
A pathogen that specializes in breaking down cellulose is not going to be well equipped
to infect animals, which had their own challenges and opportunities from the perspective of a
(04:44):
pathogen.
Now back to Harold Floor.
What was unique about his approach was that he considered the genetics of the host
flax plant and the infecting fungus together.
By studying careful pairings of crop cultivar and fungal strain, he found alleles that in
the correct combination on both sides led to a total resistance of the crop to the fungus.
(05:09):
There was some gene in the plant and some matching gene in the fungus, and when each had the right
allele combinations, then a fungal infection would be swiftly shut down by the plant, complete
resistance.
What he correctly realized and then promoted an idea is that there are genes in plants that
recognize something produced by a specific corresponding gene in the pathogen, a gene for
(05:32):
gene interaction.
The same fungal strain could infect a different cultivar, meaning plant hosts that had a different
allele of the resistance gene.
The same cultivar would succumb to a different strain, something of the genetics of each partner,
the strain of pathogen, the cultivar of the plant, functioned in response to the other,
a gene in the plant for a gene in the pathogen.
(05:55):
At the time this was a mysterious but compelling line of inquiry that would spawn a new area
of plant breeding, decades before anybody knew what these genes did, meaning what proteins
they encoded and how they worked.
Since the molecular details of plant immune systems began to be unraveled in the 1980s, it's
maybe no surprise that the first ever GMO crop, the Flaviseva tomato, hijax, a process central
(06:19):
to plant immunity.
So if we'll excuse the indulgence, we'll take a brief stop on our journey through the
science of GMOs to explore the science of plant immunity to understand both why plant
immune processes matter so much to farmers and those who develop new crop varieties,
as well as why genes are a good raw material to work with in the battle against crop
diseases.
(06:40):
Welcome to Modified, I'm your host Dr. Orlando D'Alanche, ex-plant scientist and current science
teacher.
This podcast is my attempt to guide you through the science of GMOs and hopefully just
enough of the history and the social context to give you a path forward in your own thinking.
And if all else fails, I hope you'll enjoy some of the surprising stories and fascinating
facts in the world of genetically modified plants.
(07:03):
This is episode 5, How Genes Keep Plants Alive.
When we look into the details, it becomes clear that plant immune systems have to work
really differently to animal ones, and particularly different to vertebrates like ourselves.
If you've learned anything about vertebrate immune systems, that includes human immune systems,
(07:23):
you'll have heard of white blood cells, a specialized set of blood cell types that carry
out all sorts of incredibly cool, complex immune functions, from engulfing and adjusting
bacteria to evolving new antibodies in real time against pathogens.
Plants don't even have blood, let alone white blood cells, but they do have a major tool
(07:44):
in their toolkit that we don't have.
Disposable Body Parts.
As humans, we get a set of limbs, organs and tissues and most of them cannot be replaced
or can only be replaced to a very limited extent.
Blood cells and skin cells replicate throughout our lives, but when you lose a hand or an
ear they are not going to grow back by themselves.
(08:04):
Plants don't have a predetermined and finite set of organs, throughout their lives they can
grow new leaves, shoots, roots, flowers and whatever else in response to changing environmental
conditions.
And one of those conditions is an infection.
Plants can bounce back from an infection that may wipe out most of their leaves and roots,
and it also gives them a tool to fight back against the pathogen.
(08:27):
They can sacrifice tissues by releasing a toxic cocktail of chemicals into their own tissues.
They may well kill their own tissue, but as long as it takes out the pathogen with it,
it stards the pathogen of any available food that it's a sacrifice worth making.
A localized burst of toxic chemicals that kills plant cells along with pathogens is called
(08:49):
a hypersensitive response.
A very rapid and intense release of toxic compounds is generally very effective at eliminating
an infection.
In nature there tends to happen on the scale of a few cells, just a microscopic patch of
cells around the exact site of an infection, but in lab conditions if you apply a large
amount of pathogen to a leaf you can see the hypersensitive response as a visible area
(09:14):
of dead, desiccated tissue.
If you're looking at a plant leaf that you think might be showing some battle scars from
an infection, you may be wondering how you tell apart lesions, aka, "dead areas" versus
hypersensitive response.
Verses lesions that are necrosis from the pathogen successfully munching its way through plant
(09:35):
cells.
One diagnostic indicator is a very sharp border between the living and dead tissue.
That tells you that it's probably a hypersensitive response, but they do all look pretty similar.
The hypersensitive response is an extreme version, and there are also gentler options that plants
can deploy, for instance secreting compounds out of their cells that will kill pathogens
(09:57):
in a more targeted way, or in a very general defense thickening cell walls and waxy cuticles
to slow down the infection by physically blocking the pathogen.
Another fun one is that many plants do not all excrete a mixture of sugar and DNA from
their root cells to form a sticky net that traps and keeps out pathogens.
(10:19):
An unexpected second use for DNA totally unrelated to its use as this carry-out information
as we've been getting to know it.
Plants have another tool that works specifically against viruses, RNA interference.
A set of proteins work together to detect viral RNA inside an infective cell and chop it
(10:39):
into pieces.
This only works against viruses because viruses are basically just genes in a shell that
can get into cells and hijack the cells in the machinery to manufacture new virus copies.
This requires the virus to inject its own genome into the cell.
Viral genome replication works a little differently to other organisms, and in the process there's
(11:00):
often a step that involves producing double stranded RNA, a form of RNA that doesn't otherwise
appear in plant cells.
That viral double stranded RNA is detected by specialized proteins in the plant cell and
processed into short RNA units that get copied and passed around to waiting proteins that
use those short RNA units as templates to seek out any viral RNA or DNA inside the cell
(11:24):
that matches the sequence of the template, attacking whatever they find.
Put a pin in that one because it'll come up again when we get into the world's first
GMO crop because that immune system, RNA interference, was actually a harness in the creation of that
GMO in a surprising way.
Putting it all together, plants do have quite a range of tools that they dispose of to prevent
(11:45):
and shut down pathogen infections.
This toolkit is so effective that most plants prevent most infections most of the time.
The same is also true for us humans, we are constantly being exposed to pathogens, and
most of the time we are easily able to defeat the pathogens.
So if plants are so good at the fening themselves, why do they not always win?
(12:06):
If you've walked around in nature or had a garden or house plants, you'll know that
plants do indeed get sick with all sorts of pathogens and that sometimes the pathogens
win.
The answer is that the pathogens do not just accept defeat, otherwise they would rapidly
disappear from the face of the earth.
A pathogen that cannot infect a host will die and will not pass on its genes, and so
(12:26):
from an evolutionary perspective we say that there is a very strong selective pressure
to develop ways to get around host defenses.
In practice that doesn't mean bacteria actively plotting seed strategies.
It means that random genetic mutations that allow the puffagen to evade host defenses
will make that mutated bacteria very successful.
(12:48):
It will multiply and become a dominant strain in the environment.
And this is actually easier for bacteria, viruses and fungi than it is for animals or
plants.
It means travel in one direction and animals and plants vertically.
That means down generations from mother cell to daughter cell, from parents to offspring.
(13:09):
In that process random mutation still happen which provides the raw material for evolution.
Vertical gene transfer is the standard shared of all organisms even viruses.
Basically DNA gets copied to the new daughter cell or offspring can have their own copy.
So many pathogens can also transfer DNA horizontally, which is a kind of catchal term for all sorts
(13:31):
of other DNA transfer mechanisms that can happen outside of cell division or reproduction
and generally involve transferring just small pieces of DNA just a few genes at a time.
For instance most bacteria and some fungi have in addition to their core genome packaged
into one or more chromosomes, little circles of DNA called plasmids.
(13:53):
These plasmids generally carry genes that are not essential for life but provide some competitive
advantage.
And these plasmids are easily passed between bacterial cells during the lifetime of the
cells in a process separate from cell division.
Examples of the sorts of genes that bacteria carry on plasmids include genes that inactivate
antibiotics.
(14:15):
And this is why antibiotic resistance can spread really quickly within populations of bacteria
as the plasmids get shared horizontally as well as being replicated in passed down vertically
during cell division.
Another kind of gene often carried on a plasmid is an effector.
Effector is a word for any gene or corresponding protein that is delivered from the pathogen
(14:38):
into the host and allows the pathogen to evade or disable host defenses.
Or even more broadly an effector is a protein that the pathogen delivers into the host and
helps the pathogen to infect the host.
It's those effectors that are key to getting around the defenses put up by plants.
To give you a mental image of what's going on, picture a plant cell.
(15:01):
It has a big thick cell wall, which is already quite a barrier.
The pathogens can squeeze or eat their way through that cell wall and then they encounter
the cell membrane, a thinner fatty barrier that is covered in various kinds of proteins.
Among those proteins are a range of receptors that have molecular locks that will recognize
(15:21):
molecules commonly associated with pathogens.
For instance, most plants have receptors in their cell membranes that are activated by
pieces of bacterial tail protein or pieces of fungal cell wall, which is made of a different
substance from plant cell walls.
When these cell membrane receptors are activated, they trigger a whole cascade of molecular
(15:43):
responses inside the cell, causing both immediate changes and also changes in gene expression
to switch the cell into defense mode, as well as releasing signals to neighboring cells
to get into defense mode themselves.
Many effector proteins released from the invading pathogen, worked by binding to and disabling
those membrane receptors of the plant cell.
(16:04):
Or, they are actually injected into the plant cell through the membrane, and once inside
the cell they can target different proteins that are involved in processing and transmitting
the signal that switches the cell into defense mode.
The number of effectors and their structures and functions is truly vast.
I did a whole PhD on just one family effector proteins, so could you buy a specific set
(16:28):
of bacterial pathogens.
Those effectors are very unusual, the ones I studied, and that they actually function as
transcription factors inside the plant cell, hijacking and redirecting gene expression
as specific target genes to benefit the invading bacteria.
If that's something you'd like to hear more about in our upcoming Q&A episode, let me know.
(16:49):
I could easily ramble on for a good hour all about those proteins, which are called
"tall effectors."
But anyway, these effector proteins are to be honest pretty cool, but plants don't
just declare defeat in this evolutionary arms race, instead plants have their own huge
array of anti-effector and mean receptors.
We can call these protein's effector detectors.
(17:12):
That's not the term used by plant pathologists, but I think the jargon load in this episode
is already really high, so effector detector is a fun word we can use.
So in addition to the core set of membrane-bound receptors that detect and respond to core pathogen molecules,
they have a much larger, more diverse set of effector detectors.
Normally patrolling on the inside of the cell, they recognize specific effector proteins,
(17:34):
and when they do, they trigger that dramatic hypersensitive response introduced earlier.
Any given plant will have a few hundred different genes encoding unique effector detectors.
That's an individual plant, but if you look at the genomes of every plant in that one
species across the world, what geneticists would call the "pan genome" of that species,
(17:57):
you would probably find a few thousand distinct effector detectors genes.
Effector detectors genes are very diverse and they evolve rapidly relative to most plant genes,
and that's because they are responding to the specific pathogens that are a problem
in the particular environment of the plant population.
(18:17):
The effector genes and the effector detector genes are locked in an evolutionary arms race.
Remember Harold Floor from right at the start of the episode, he was the one who first articulated
the idea that there were gene for gene interactions with the specific effector genes in pathogens
and corresponding effector detector genes in plants, and that they were very variable
(18:39):
and diverse between different populations of plants and pathogens.
Hundreds of different proteins encoded by hundreds of different genes.
When he shared his idea, it sparked a flurry of activity which continues to this day,
with academic researchers investigating effector genes and their corresponding plant resistance
genes counterparts.
And that research doesn't just get published in academic journals or it sits unused and
(19:01):
unread, an industry of commercial and government plant breeders build on that information to
develop new disease resistant crop varieties.
Every year 40% of the crops grown globally are lost to insects and pathogens, with an estimated
value of 220 billion. That's according to a 2022 report from the UN Food and Agriculture
(19:22):
Organization.
And I know I didn't actually mention insects so far, but I'll just summarize in a sentence
that most of what it described for how plants protect themselves against pathogens also
applies to insect pests.
Basically pests and pathogens are devastating and very expensive problem for farmers.
And the stakes are significantly higher in the agricultural systems now prevalent across
(19:44):
much of the world. In any given region, you will likely find just a few major crops grown
and of those you will likely find that many farmers are growing fields of genetically identical
plants, also known as monocultures.
As all see in future episodes, monocultures are a modern phenomenon. They take a lot of
work to achieve because genetic variation is the norm for plants that reproduce via
(20:07):
sexual reproduction, which is most of our crop plants.
Some crops can be and have long been grown via cuttings, which just produce genetically
identical offspring because the cuttings are just like branches of the same mother plant.
Plants long grown from cuttings includes most fruit trees.
A non-tree example is potatoes, where generally potato tubers are planted to grow new potato
(20:30):
plants, even though potato plants do produce flowers and seeds. Like I said, there are advantages
to growing genetically identical fields of crops, so historically, where this has been
easy to achieve, it was done, even before people had a concept of genes.
People could still observe that planting potato always gives a plant identical to the one
that produced the potato, while planting seeds from the plant would give you variation
(20:55):
in the offspring. An identical offspring means you can predict what you'll be harvesting
next season and how those plants will respond to environmental conditions.
So even though farmers have long valued genetic uniformity, the scale of monoculture and
today's agricultural systems is unprecedented. And so if a new disease appears on the scene
that can kill a commonly grown cultivar in a region, then you'll have a lot of farmers
(21:18):
whose livelihoods are now on the line, and major disruptions to food prices, which can
lead to people not being able to afford to eat, or at least eat what they'd like to.
So unsurprisingly, this is not something that governments just leave up to the free market
to manage. Most countries have some sort of government-funded monitoring system to keep
track of prevalent pests and pathogens and detect new threats early. When a new threat is detected,
(21:42):
sometimes there are ways to deal with this without changing the cultivars being grown. For example,
by spraying with particular pesticides if the threat is an insect. But generally plant
breeding is part of the solution. I mean the government run labs, academic labs, and private
for-profit plant breeding companies will rapidly look for resistance genes, often those affected
detectors that might exist somewhere in the total diversity, total genetic diversity of
(22:08):
that crop, and then breed that gene and that trait into the cultivar that is favored
in the region in question. And we'll peer more into how that process works in future episodes.
But what if there really is nothing already available within the net-actual genetic variation
of the crop, or any of its close-wild relatives that would work against the particular pathogen?
Or perhaps you're working with a plant like a tree fruit crop that is very slow and difficult
(22:32):
to do traditional plant breeding with. That's exactly the situation that faced the Hawaii
papaya industry in the 1990s because of the papaya "ringspot" virus.
The virus isn't just to figure the fruit, it kills the plants. The virus arrived in the
Hawaiian Islands in the 1930s and thus began a game of cat and mouse with papaya cultivation
(22:54):
moving around the islands until by the 1980s there was nowhere safe left and the industries
seemed to be finished. There was no option to repapy her that were resistant to the virus.
But by the 1980s, nearly a century of genetics and molecular biology had yielded new options.
And so, plant scientists, Teneegon Zalves from Hawaii originally but working at Cornell University
(23:20):
tested what happened if he used pieces of the virus's own genome to create a new synthetic
gene that could be inserted into the papaya genome to trigger RNA interference protecting
against the virus. It worked. From the brink of disappearing, the Hawaii papaya industry
recovered with 11 million pounds of papaya's grown commercially in the state in 2024.
(23:43):
The vast majority of these papayas are from GMO papayatries.
If you want to learn more about the story of Teneegon Zalves and the GMO papayas, then keep
listening to 'Modified' by me or landed lunch, but we'll end this episode here.
Keep listening for today's five take home messages. And if not, I hope you'll tune in again
(24:03):
in a few weeks for a special Q&A episode before we shift gears of the second part of season
one focusing on crops agriculture and what it takes to create a GMO.
Theory of Take Home Messages One, pathogens are microorganisms that can infect
hosts to cause a disease. Two, major pathogen groups affecting plants are bacteria, fungi,
(24:25):
viruses and umi seeds. Number three, hundreds of genes within any given plant genome
encode proteins specifically devoted to defending against pathogens.
Number four, pathogens produce affector proteins to disable host proteins and plants have their
own affected detectors to trigger a hyperspensitive response and the presence of a matching effector.
(24:49):
Five, genes that provide resistance to pathogens are major targets for plant breeding efforts
and this includes developing GMO crops with totally novel resistance genes.
Thank you for listening to 'Modified'. This was episode five, 'How Genes Keep Plants Alive'
is written by me or landed lunch. I use many sources to help me research this episode.
(25:10):
I want to particularly acknowledge 'HH Floor' a pioneer in phytopathology by Leo Garrig
and Elling Bowie. In a week I'll be reviewing all the questions sent into me so far to put
together a special Q&A episode of this podcast as a little interlude before we continue with
the season so there's still time to get your questions in.
You can submit questions to Orlando@modified.com that's O-R-L-A-N-D-O at ModifiedPod.com or
(25:37):
you can send them to me on Blue Sky or Instagram. Handles are on the website for the podcast
which is just 'modifiedpod.com'. This is a tiny one person podcast so please please if you're
enjoying it leave a review, subscribe and tell a friend. It really really helps and I appreciate
it. With that, thanks for listening. Bye!
[Music]
The spores of the Flax Rust fungus keep very well in the refrigerator.
(00:04):
That's a mundane discovery that Harold Floor made as he went about his research, but
as so often in science, the mundane details can be what paves the way for major discoveries.
Harold Floor was an unassuming man.
A plant scientist working from the 1920s to the 1980s, he was born in St. Paul, Minnesota.
(00:25):
He loved hunting and fishing, and he didn't seem to care much for teaching or for mentoring
new students.
To be honest, from other things I've read about him, I can't say that I think Harold
and I would have had very much in common.
But there is at least one thing we had in common, a love of plant pathology.
Plant pathology is the study of plant diseases, plant immune systems, and had to protect crop
(00:45):
plants against diseases.
It is a field that Dr Floor dedicated his entire long career to, whereas I only dedicated
the five years of my PhD studies to it.
But this specific area of plant pathology that I worked on ultimately rests on Dr Floor's
discoveries, that is the study of plant pathogen effector proteins and the plant resistance
(01:06):
genes that defend against them.
Harold Floor's most impactful contribution wasn't so much any one factor finding though
he certainly made thousands and thousands of careful observations of fungal pathogens
of plant hosts, particularly the Flax plant and how they interact.
He would watch with practice patients as the tiny yellow proliferation of fungal mass would
(01:29):
grow at each infection site, spread across the leaf and eventually killed the leaf.
And he would watch just as closely with the help of a microscope how sometimes the spores
of the fungus would germinate, stretch out a hopeful, hyphil thread only to weather and
die, leaving a healthy leaf unbothered by the fungal threat.
And as he carefully tracked the results of these experiments over years, something started
(01:53):
to become clear to him.
He compared the results of these experiments to the conceptual models emerging in the 1930s
and 40s from the field of genetics, which by that point had grown over several decades
to become arguably the hottest field in life science.
Genetics had become a major part of the biological science mainstream and that had catalyzed
(02:13):
the explosion of plant breeding as we'll see in our next episode.
Harold Floor was not by any means the first person to try to use the tools of genetics
to understand plant diseases, and more specifically how some plants are able to resist disease
while others succumb.
It was already well established that there were genes that influence plant disease, resistance
(02:33):
and infection, with more resistant and less resistant alleles of these genes found.
It was already known that in most cases these genes were specific in their effect to certain
pathogen types.
And of course it was known that the pathogens themselves, whether they be bacteria, fungi
or viruses have their own genes and that certain pathogen genes affect how well they can
(02:56):
infect a host.
You may never have thought about it, but plants can be infected by the same sorts of organisms
as animals, including ourselves.
Though not generally the same species or strains, a virus that can infect plants won't be
able to infect animals and vice versa.
Fungai are much more of a problem for plants than they are for animals, with some of the most
(03:17):
devastating crop diseases caused by fungi.
Plants are also particularly plagued by the superficially fungus-like microorganisms called
"Umei seeds".
A famous example is Phytophthoro-infestans, the pathogen that caused potato crops to fail
in the 1840s in Ireland, which in the context of British colonial rule triggered a massive
(03:38):
and deadly famine.
There are some Umei seeds that infect humans, but overall Umei seeds are more of a plant
thing.
Plant tissues like animal tissues are stores of energy in biomolecules, a perfect food for
a hungry pathogen to feed on, grow and divide, and so microorganisms will try to invade and
(03:58):
get that energy and those nutrients.
We call that process an infection, and we call the organisms doing the infecting pathogens,
and that implies whether the infected host is a human or a hydrangea.
However, the particulars of plant biology do lead to some major differences when it comes
to thinking about how the experience and fight infections.
(04:20):
For instance, plant tissues are full of cellulose, and molecule that animals don't have.
Cellulose cell walls are both a major barrier in the way of pathogens, and a potential
source of energy for those able to break them down and digest them.
A pathogen that specializes in breaking down cellulose is not going to be well equipped
to infect animals, which had their own challenges and opportunities from the perspective of a
(04:44):
pathogen.
Now back to Harold Floor.
What was unique about his approach was that he considered the genetics of the host
flax plant and the infecting fungus together.
By studying careful pairings of crop cultivar and fungal strain, he found alleles that in
the correct combination on both sides led to a total resistance of the crop to the fungus.
(05:09):
There was some gene in the plant and some matching gene in the fungus, and when each had the right
allele combinations, then a fungal infection would be swiftly shut down by the plant, complete
resistance.
What he correctly realized and then promoted an idea is that there are genes in plants that
recognize something produced by a specific corresponding gene in the pathogen, a gene for
(05:32):
gene interaction.
The same fungal strain could infect a different cultivar, meaning plant hosts that had a different
allele of the resistance gene.
The same cultivar would succumb to a different strain, something of the genetics of each partner,
the strain of pathogen, the cultivar of the plant, functioned in response to the other,
a gene in the plant for a gene in the pathogen.
(05:55):
At the time this was a mysterious but compelling line of inquiry that would spawn a new area
of plant breeding, decades before anybody knew what these genes did, meaning what proteins
they encoded and how they worked.
Since the molecular details of plant immune systems began to be unraveled in the 1980s, it's
maybe no surprise that the first ever GMO crop, the Flaviseva tomato, hijax, a process central
(06:19):
to plant immunity.
So if we'll excuse the indulgence, we'll take a brief stop on our journey through the
science of GMOs to explore the science of plant immunity to understand both why plant
immune processes matter so much to farmers and those who develop new crop varieties,
as well as why genes are a good raw material to work with in the battle against crop
diseases.
(06:40):
Welcome to Modified, I'm your host Dr. Orlando D'Alanche, ex-plant scientist and current science
teacher.
This podcast is my attempt to guide you through the science of GMOs and hopefully just
enough of the history and the social context to give you a path forward in your own thinking.
And if all else fails, I hope you'll enjoy some of the surprising stories and fascinating
facts in the world of genetically modified plants.
(07:03):
This is episode 5, How Genes Keep Plants Alive.
When we look into the details, it becomes clear that plant immune systems have to work
really differently to animal ones, and particularly different to vertebrates like ourselves.
If you've learned anything about vertebrate immune systems, that includes human immune systems,
(07:23):
you'll have heard of white blood cells, a specialized set of blood cell types that carry
out all sorts of incredibly cool, complex immune functions, from engulfing and adjusting
bacteria to evolving new antibodies in real time against pathogens.
Plants don't even have blood, let alone white blood cells, but they do have a major tool
(07:44):
in their toolkit that we don't have.
Disposable Body Parts.
As humans, we get a set of limbs, organs and tissues and most of them cannot be replaced
or can only be replaced to a very limited extent.
Blood cells and skin cells replicate throughout our lives, but when you lose a hand or an
ear they are not going to grow back by themselves.
(08:04):
Plants don't have a predetermined and finite set of organs, throughout their lives they can
grow new leaves, shoots, roots, flowers and whatever else in response to changing environmental
conditions.
And one of those conditions is an infection.
Plants can bounce back from an infection that may wipe out most of their leaves and roots,
and it also gives them a tool to fight back against the pathogen.
(08:27):
They can sacrifice tissues by releasing a toxic cocktail of chemicals into their own tissues.
They may well kill their own tissue, but as long as it takes out the pathogen with it,
it stards the pathogen of any available food that it's a sacrifice worth making.
A localized burst of toxic chemicals that kills plant cells along with pathogens is called
(08:49):
a hypersensitive response.
A very rapid and intense release of toxic compounds is generally very effective at eliminating
an infection.
In nature there tends to happen on the scale of a few cells, just a microscopic patch of
cells around the exact site of an infection, but in lab conditions if you apply a large
amount of pathogen to a leaf you can see the hypersensitive response as a visible area
(09:14):
of dead, desiccated tissue.
If you're looking at a plant leaf that you think might be showing some battle scars from
an infection, you may be wondering how you tell apart lesions, aka, "dead areas" versus
hypersensitive response.
Verses lesions that are necrosis from the pathogen successfully munching its way through plant
(09:35):
cells.
One diagnostic indicator is a very sharp border between the living and dead tissue.
That tells you that it's probably a hypersensitive response, but they do all look pretty similar.
The hypersensitive response is an extreme version, and there are also gentler options that plants
can deploy, for instance secreting compounds out of their cells that will kill pathogens
(09:57):
in a more targeted way, or in a very general defense thickening cell walls and waxy cuticles
to slow down the infection by physically blocking the pathogen.
Another fun one is that many plants do not all excrete a mixture of sugar and DNA from
their root cells to form a sticky net that traps and keeps out pathogens.
(10:19):
An unexpected second use for DNA totally unrelated to its use as this carry-out information
as we've been getting to know it.
Plants have another tool that works specifically against viruses, RNA interference.
A set of proteins work together to detect viral RNA inside an infective cell and chop it
(10:39):
into pieces.
This only works against viruses because viruses are basically just genes in a shell that
can get into cells and hijack the cells in the machinery to manufacture new virus copies.
This requires the virus to inject its own genome into the cell.
Viral genome replication works a little differently to other organisms, and in the process there's
(11:00):
often a step that involves producing double stranded RNA, a form of RNA that doesn't otherwise
appear in plant cells.
That viral double stranded RNA is detected by specialized proteins in the plant cell and
processed into short RNA units that get copied and passed around to waiting proteins that
use those short RNA units as templates to seek out any viral RNA or DNA inside the cell
(11:24):
that matches the sequence of the template, attacking whatever they find.
Put a pin in that one because it'll come up again when we get into the world's first
GMO crop because that immune system, RNA interference, was actually a harness in the creation of that
GMO in a surprising way.
Putting it all together, plants do have quite a range of tools that they dispose of to prevent
(11:45):
and shut down pathogen infections.
This toolkit is so effective that most plants prevent most infections most of the time.
The same is also true for us humans, we are constantly being exposed to pathogens, and
most of the time we are easily able to defeat the pathogens.
So if plants are so good at the fening themselves, why do they not always win?
(12:06):
If you've walked around in nature or had a garden or house plants, you'll know that
plants do indeed get sick with all sorts of pathogens and that sometimes the pathogens
win.
The answer is that the pathogens do not just accept defeat, otherwise they would rapidly
disappear from the face of the earth.
A pathogen that cannot infect a host will die and will not pass on its genes, and so
(12:26):
from an evolutionary perspective we say that there is a very strong selective pressure
to develop ways to get around host defenses.
In practice that doesn't mean bacteria actively plotting seed strategies.
It means that random genetic mutations that allow the puffagen to evade host defenses
will make that mutated bacteria very successful.
(12:48):
It will multiply and become a dominant strain in the environment.
And this is actually easier for bacteria, viruses and fungi than it is for animals or
plants.
It means travel in one direction and animals and plants vertically.
That means down generations from mother cell to daughter cell, from parents to offspring.
(13:09):
In that process random mutation still happen which provides the raw material for evolution.
Vertical gene transfer is the standard shared of all organisms even viruses.
Basically DNA gets copied to the new daughter cell or offspring can have their own copy.
So many pathogens can also transfer DNA horizontally, which is a kind of catchal term for all sorts
(13:31):
of other DNA transfer mechanisms that can happen outside of cell division or reproduction
and generally involve transferring just small pieces of DNA just a few genes at a time.
For instance most bacteria and some fungi have in addition to their core genome packaged
into one or more chromosomes, little circles of DNA called plasmids.
(13:53):
These plasmids generally carry genes that are not essential for life but provide some competitive
advantage.
And these plasmids are easily passed between bacterial cells during the lifetime of the
cells in a process separate from cell division.
Examples of the sorts of genes that bacteria carry on plasmids include genes that inactivate
antibiotics.
(14:15):
And this is why antibiotic resistance can spread really quickly within populations of bacteria
as the plasmids get shared horizontally as well as being replicated in passed down vertically
during cell division.
Another kind of gene often carried on a plasmid is an effector.
Effector is a word for any gene or corresponding protein that is delivered from the pathogen
(14:38):
into the host and allows the pathogen to evade or disable host defenses.
Or even more broadly an effector is a protein that the pathogen delivers into the host and
helps the pathogen to infect the host.
It's those effectors that are key to getting around the defenses put up by plants.
To give you a mental image of what's going on, picture a plant cell.
(15:01):
It has a big thick cell wall, which is already quite a barrier.
The pathogens can squeeze or eat their way through that cell wall and then they encounter
the cell membrane, a thinner fatty barrier that is covered in various kinds of proteins.
Among those proteins are a range of receptors that have molecular locks that will recognize
(15:21):
molecules commonly associated with pathogens.
For instance, most plants have receptors in their cell membranes that are activated by
pieces of bacterial tail protein or pieces of fungal cell wall, which is made of a different
substance from plant cell walls.
When these cell membrane receptors are activated, they trigger a whole cascade of molecular
(15:43):
responses inside the cell, causing both immediate changes and also changes in gene expression
to switch the cell into defense mode, as well as releasing signals to neighboring cells
to get into defense mode themselves.
Many effector proteins released from the invading pathogen, worked by binding to and disabling
those membrane receptors of the plant cell.
(16:04):
Or, they are actually injected into the plant cell through the membrane, and once inside
the cell they can target different proteins that are involved in processing and transmitting
the signal that switches the cell into defense mode.
The number of effectors and their structures and functions is truly vast.
I did a whole PhD on just one family effector proteins, so could you buy a specific set
(16:28):
of bacterial pathogens.
Those effectors are very unusual, the ones I studied, and that they actually function as
transcription factors inside the plant cell, hijacking and redirecting gene expression
as specific target genes to benefit the invading bacteria.
If that's something you'd like to hear more about in our upcoming Q&A episode, let me know.
(16:49):
I could easily ramble on for a good hour all about those proteins, which are called
"tall effectors."
But anyway, these effector proteins are to be honest pretty cool, but plants don't
just declare defeat in this evolutionary arms race, instead plants have their own huge
array of anti-effector and mean receptors.
We can call these protein's effector detectors.
(17:12):
That's not the term used by plant pathologists, but I think the jargon load in this episode
is already really high, so effector detector is a fun word we can use.
So in addition to the core set of membrane-bound receptors that detect and respond to core pathogen molecules,
they have a much larger, more diverse set of effector detectors.
Normally patrolling on the inside of the cell, they recognize specific effector proteins,
(17:34):
and when they do, they trigger that dramatic hypersensitive response introduced earlier.
Any given plant will have a few hundred different genes encoding unique effector detectors.
That's an individual plant, but if you look at the genomes of every plant in that one
species across the world, what geneticists would call the "pan genome" of that species,
(17:57):
you would probably find a few thousand distinct effector detectors genes.
Effector detectors genes are very diverse and they evolve rapidly relative to most plant genes,
and that's because they are responding to the specific pathogens that are a problem
in the particular environment of the plant population.
(18:17):
The effector genes and the effector detector genes are locked in an evolutionary arms race.
Remember Harold Floor from right at the start of the episode, he was the one who first articulated
the idea that there were gene for gene interactions with the specific effector genes in pathogens
and corresponding effector detector genes in plants, and that they were very variable
(18:39):
and diverse between different populations of plants and pathogens.
Hundreds of different proteins encoded by hundreds of different genes.
When he shared his idea, it sparked a flurry of activity which continues to this day,
with academic researchers investigating effector genes and their corresponding plant resistance
genes counterparts.
And that research doesn't just get published in academic journals or it sits unused and
(19:01):
unread, an industry of commercial and government plant breeders build on that information to
develop new disease resistant crop varieties.
Every year 40% of the crops grown globally are lost to insects and pathogens, with an estimated
value of 220 billion. That's according to a 2022 report from the UN Food and Agriculture
(19:22):
Organization.
And I know I didn't actually mention insects so far, but I'll just summarize in a sentence
that most of what it described for how plants protect themselves against pathogens also
applies to insect pests.
Basically pests and pathogens are devastating and very expensive problem for farmers.
And the stakes are significantly higher in the agricultural systems now prevalent across
(19:44):
much of the world. In any given region, you will likely find just a few major crops grown
and of those you will likely find that many farmers are growing fields of genetically identical
plants, also known as monocultures.
As all see in future episodes, monocultures are a modern phenomenon. They take a lot of
work to achieve because genetic variation is the norm for plants that reproduce via
(20:07):
sexual reproduction, which is most of our crop plants.
Some crops can be and have long been grown via cuttings, which just produce genetically
identical offspring because the cuttings are just like branches of the same mother plant.
Plants long grown from cuttings includes most fruit trees.
A non-tree example is potatoes, where generally potato tubers are planted to grow new potato
(20:30):
plants, even though potato plants do produce flowers and seeds. Like I said, there are advantages
to growing genetically identical fields of crops, so historically, where this has been
easy to achieve, it was done, even before people had a concept of genes.
People could still observe that planting potato always gives a plant identical to the one
that produced the potato, while planting seeds from the plant would give you variation
(20:55):
in the offspring. An identical offspring means you can predict what you'll be harvesting
next season and how those plants will respond to environmental conditions.
So even though farmers have long valued genetic uniformity, the scale of monoculture and
today's agricultural systems is unprecedented. And so if a new disease appears on the scene
that can kill a commonly grown cultivar in a region, then you'll have a lot of farmers
(21:18):
whose livelihoods are now on the line, and major disruptions to food prices, which can
lead to people not being able to afford to eat, or at least eat what they'd like to.
So unsurprisingly, this is not something that governments just leave up to the free market
to manage. Most countries have some sort of government-funded monitoring system to keep
track of prevalent pests and pathogens and detect new threats early. When a new threat is detected,
(21:42):
sometimes there are ways to deal with this without changing the cultivars being grown. For example,
by spraying with particular pesticides if the threat is an insect. But generally plant
breeding is part of the solution. I mean the government run labs, academic labs, and private
for-profit plant breeding companies will rapidly look for resistance genes, often those affected
detectors that might exist somewhere in the total diversity, total genetic diversity of
(22:08):
that crop, and then breed that gene and that trait into the cultivar that is favored
in the region in question. And we'll peer more into how that process works in future episodes.
But what if there really is nothing already available within the net-actual genetic variation
of the crop, or any of its close-wild relatives that would work against the particular pathogen?
Or perhaps you're working with a plant like a tree fruit crop that is very slow and difficult
(22:32):
to do traditional plant breeding with. That's exactly the situation that faced the Hawaii
papaya industry in the 1990s because of the papaya "ringspot" virus.
The virus isn't just to figure the fruit, it kills the plants. The virus arrived in the
Hawaiian Islands in the 1930s and thus began a game of cat and mouse with papaya cultivation
(22:54):
moving around the islands until by the 1980s there was nowhere safe left and the industries
seemed to be finished. There was no option to repapy her that were resistant to the virus.
But by the 1980s, nearly a century of genetics and molecular biology had yielded new options.
And so, plant scientists, Teneegon Zalves from Hawaii originally but working at Cornell University
(23:20):
tested what happened if he used pieces of the virus's own genome to create a new synthetic
gene that could be inserted into the papaya genome to trigger RNA interference protecting
against the virus. It worked. From the brink of disappearing, the Hawaii papaya industry
recovered with 11 million pounds of papaya's grown commercially in the state in 2024.
(23:43):
The vast majority of these papayas are from GMO papayatries.
If you want to learn more about the story of Teneegon Zalves and the GMO papayas, then keep
listening to 'Modified' by me or landed lunch, but we'll end this episode here.
Keep listening for today's five take home messages. And if not, I hope you'll tune in again
(24:03):
in a few weeks for a special Q&A episode before we shift gears of the second part of season
one focusing on crops agriculture and what it takes to create a GMO.
Theory of Take Home Messages One, pathogens are microorganisms that can infect
hosts to cause a disease. Two, major pathogen groups affecting plants are bacteria, fungi,
(24:25):
viruses and umi seeds. Number three, hundreds of genes within any given plant genome
encode proteins specifically devoted to defending against pathogens.
Number four, pathogens produce affector proteins to disable host proteins and plants have their
own affected detectors to trigger a hyperspensitive response and the presence of a matching effector.
(24:49):
Five, genes that provide resistance to pathogens are major targets for plant breeding efforts
and this includes developing GMO crops with totally novel resistance genes.
Thank you for listening to 'Modified'. This was episode five, 'How Genes Keep Plants Alive'
is written by me or landed lunch. I use many sources to help me research this episode.
(25:10):
I want to particularly acknowledge 'HH Floor' a pioneer in phytopathology by Leo Garrig
and Elling Bowie. In a week I'll be reviewing all the questions sent into me so far to put
together a special Q&A episode of this podcast as a little interlude before we continue with
the season so there's still time to get your questions in.
You can submit questions to Orlando@modified.com that's O-R-L-A-N-D-O at ModifiedPod.com or
(25:37):
you can send them to me on Blue Sky or Instagram. Handles are on the website for the podcast
which is just 'modifiedpod.com'. This is a tiny one person podcast so please please if you're
enjoying it leave a review, subscribe and tell a friend. It really really helps and I appreciate
it. With that, thanks for listening. Bye!
[Music]
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