Chapter 23: Ustilaginomycetes: Smut Fungi and Allies

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Have you ever thought about the hidden players in the plant world, the ones working behind the scenes, transforming things?

Hmm, like tiny puppet masters.

Exactly.

Today, we're diving deep into oestilogenomycetes.

You might know them as smut fungi, along with their, well, surprising fungal cousins.

Yeah, and these aren't just some obscure group, they're incredibly diverse masters of plant manipulation, really.

And they pop up everywhere, agriculture, ecosystems,

even, believe it or not, in some cuisines.

We're exploring a chapter from Webster and Weber's Introduction to Fungi.

Right.

Our goal is to break down all this complex science, make it engaging,

memorable, without needing any pictures.

So this group, oestilogenomycetes,

part of the city of Mycota, right, about 1 ,500 species.

That's the one.

And they really show this fascinating duality fungi as essential ecosystem parts, but also, you know, pretty powerful plant pathogens.

It's all about these intricate biological tricks and their real world consequences.

Okay, let's unpack that.

Oestilogenomycetes.

What makes them so, well, special in the fungal kingdom?

Fundamentally, they're one of the four main classes of Basidiomycota, a monophyletic group, meaning they all share a common ancestor.

Got it.

And their lifestyle.

Mostly plant pathogens.

Ecologically obligate plant pathogens, yes, they have to live on plants for part of their life.

But here's a key thing.

Many also have this free -living yeast phase.

Ah, the dimorphism, so they can switch between forms.

Precisely.

Yeast -like, living on dead stuff, or mycelial thread -like, and infecting plants.

That switch is crucial for them.

And how do they differ from, say, their close relatives, the rust fungi,

microscopically?

Good question.

There are specific differences.

Take Hostoria, those specialized feeding structures.

Smuts either don't have them or they have really simple ones.

So not like the invasive structures in rusts.

Right.

Smuts often just invaginate the host cell membrane, gently push into it almost, and their internal hyphal walls, the septa, they have simple pores, or none, but critically they lack parenthesomes.

Parenthesomes.

Those are the little cap -like structures found around the pores and many other basidiomycota.

Exactly.

Smuts don't have those.

You also don't usually find true clamp connections, which are common elsewhere in this phylum.

Okay.

And spore production.

Smuts produce loads of basidiospores, whereas rusts typically just make four.

Little details, but they add up to define the group.

So when we say smut fungus, it's often describing the symptoms we see, rather than being a strict taxonomic label.

That's a really important point, yeah.

Some fungi that cause smut -like symptoms are actually rusts, taxonomically speaking.

It shows how fungi don't always fit neatly into boxes based on appearance alone.

Makes sense.

Within the Ostalaginomycetes class itself, are there subgroups?

Yes.

Three main subclasses.

The Ostalaginomycetidae are the big ones, the classic plant pathogens causing those smut -like symptoms.

Then there's the Exobasidiomycetidae, causing other types of diseases, and the Enterizomycetidae, which make galls on roots of specific plants like sedges and rushes.

Okay.

Let's focus on those main ones.

The Ostalaginomycetidae.

What are these classic smut symptoms they're named after?

What do they look like?

All right.

Smut refers to the fungus or the disease.

And the key feature is these masses, called sori, of dark, powdery spores that erupt from infected plant parts.

Like soot or, well, smut.

Exactly.

Leaves, stems, flowers, seeds, especially in grasses, are common targets.

You might also hear the term bunt.

Bunt.

How's that different?

Bunt is often used when the fungus infects the ovaries, so the developing seed gets completely filled with spores instead of an embryo.

Visually, the tissues around where the spores burst out often look burnt or scorched.

Ah.

Hence the old German name, Brandpil's fire fungi.

Precisely.

And those dark spores.

They have many names, Chlamydospore, Brandspore, Otoospore, but the preferred scientific term is Teliospore.

Why Teliospore specifically?

Because its function is the same as the Teliospore in rust fungi.

It's the site where the two parental nuclei fuse, becoming deployed.

Then, when it germinates, it forms a structure called a promycelium, where meiosis happens, creating the haploid spores that start the next generation.

Okay, so that brings us to their life cycle.

You mentioned it's a tale of two phases, the dimorphic dance.

Absolutely.

You have the monocariotic phase haploid, yeast -like.

It can grow saprotrophically, meaning on dead organic matter, just fine.

But crucially, it cannot infect a living plant.

And the other phase?

That's the dicariotic phase.

It's mostly mycelial, those thread -like hyphae.

This phase is infectious, it's the parasite, but, and this is key, it generally cannot grow saprotrophically on its own in the environment.

It needs the host.

So how do they make the switch from harmless yeast to infectious mycelium?

It starts with those haploid basidiospores, often called spyridia, butting off the promycelium.

These can multiply as yeast cells, living freely for a while.

But infection only happens when two compatible yeast cells meet on the host plant's surface.

Compatible, like different mating types.

Exactly.

When compatible cells meet, they fuse.

That fusion event creates the dicariotic cell, which then grows as the infectious hypha.

And this infectious hypha gets into the plant.

Yes.

It often grows systemically, spreading throughout the plant, sometimes between cells, sometimes penetrating them.

It especially likes actively growing tissues, like meristems.

Does it form those hostoria we talked about?

Usually not specialized ones.

The hyphae might enter host cells, invaginating the membrane, and they often get surrounded by this sheath material made by both the fungus and the plant.

It's an intimate connection.

And then eventually the spores form.

The smut.

Right.

In the areas where the source will form, the dicariotic hyphae multiply rapidly, forming dense masses.

They often destroy the softer host tissues inside, but stay contained by the plant's outer layer, the epidermis, for a while.

Then, most of these hyphal segments convert into teliospores.

The two nuclei in each segment fuse.

The walls thicken, often darken, and sometimes get ornamented, and boom, you have a mass of mature teliospores ready to be released.

It's quite a sophisticated process.

But how do they guarantee finding a compatible partner for that initial fusion?

It sounds like a bottleneck.

It relies on their mating systems.

Many are heterothallic.

They need two different mating types.

The simplest is a bipolar system.

Basically, one gene with two versions, like an on -off switch.

Like an ustelago hordei, the barley smut.

Yes.

But some, like the famous ustelago mateys corn smut, are tetrapolar.

They have two different mating type locations, or loci, on different chromosomes.

It's more complex.

Two loci.

How does that work?

Well, one locus, called the A locus, has two versions, A1 and A2.

Each produces a specific pheromone, a chemical signal, and also the receptor for the other type's pheromone.

So they can smell each other.

Kind of.

When a cell detects the pheromone from a compatible partner, it stops dividing and grows the thin tube towards the signal source.

This A locus basically controls the fusion event itself.

Okay, that's locus A.

What about locus B?

The B locus is different.

It has many versions, maybe 25 or so in mateys.

This one controls the outcome of the fusion, the ability of the resulting decaryon to grow properly, be pathogenic, and complete the sexual cycle.

How does it do that?

Each B allele encodes two proteins.

Let's call them B and BW.

For the decaryon to be pathogenic, it needs to have proteins from different B alleles.

For example, BE1 and BW2 can pair up, but BE1 and BW1 can't.

This paired up unit acts as a master switch, a transcription factor, turning on genes needed for the parasitic lifestyle.

Wow, that's intricate.

Like a double -lock system, A for fusion, B for successful infection.

Exactly.

And interestingly, in those simpler bipolar species like U hordei, the A and B loci are physically linked together on the chromosome, and they don't recombine much.

Some see this as a sort of primitive sex chromosome.

And this whole dimorphic switching ability, it's made them useful in research, right?

Yeah.

Especially in stalagomates.

Hugely useful.

The ability to easily switch between a culturable yeast phase and the infectious hyphol phase makes it a fantastic model for studying basic cell biology, things like cell shape, signaling, how things move around inside cells.

So once these tough taliospores are formed, how do they get out and about?

Dispersal.

Usually, they're released dry when the host tissue covering the sorus ruptures.

This might be just pressure from the spores, or helped along by wind shaking the plant, or even rain splash.

Or the whole infected bit breaks off.

Sometimes, yes.

Wind is the big one for long distance.

They think African sugarcane smut spore is actually blue across the Atlantic.

Seriously, wow.

Yeah.

And many stick to host seeds.

So when the farmer sows the seed, they sow the fungus too.

Human transport of contaminated grain is obviously a huge factor in spreading them globally.

Any other ways?

Oh yeah.

Some rely on insects.

Like the anthersmut, Microbotrium violacium, uses pollinators to move its spores flower to flower.

Okay, let's look at some specific examples.

Starting with the ustelago species that hit our cereal crops.

Several ustelago species are major pathogens of grasses and cereals.

They often replace the developing seeds with their sori.

Take ustelago horde, the covered smut of barley and oats.

It's the type species for the genus.

Covered, meaning the spores stay inside the grain.

Inside the outer layers, yes.

They're mostly released during threshing, contaminating healthy seeds.

When those seeds are planted, the spores germinate, compatible yeast cells fuse, form the infectious hypha and infect the seedling.

And then it hides inside the plant for a while.

Exactly.

There's this long systemic growth phase with no outward symptoms.

The fungus mainly grows inside the host cells.

It only really ramps up proliferation when it reaches the growing tip, the apical meristem, and then it fills the developing flower parts, the spikelets, with hyphae that become tiliospores.

That delayed symptom development is classic for many small grain cereal smuts.

So the farmer might not know until harvest time.

What about the loose smuts, like ustelago avani on oats, or eunuda and eutritici on barley and wheat?

With loose smuts, it's much more obvious earlier.

The kernels are visibly replaced by powdery spore masses, and often the surrounding structures, the glooms, are destroyed too.

And how do they spread differently from covered smuts?

Yes, there are differences.

Eue avinae tiliospores are tough.

They can survive for like 13 years.

They can infect seedlings from spores just dusting the outside of the sea, or sometimes via a limited infection within the seed code itself.

But the barley and wheat loose smuts, eunuda and eutritici.

Their tiliospores are very short -lived, often just days.

So surface contamination isn't the main route.

For them, infection happens primarily at flowering time.

Spores from a smutted plant land on a healthy flower, germinate, and infect the young tissues at the base of the ovary.

The fungus then grows into the developing embryo and waits there, dormant, inside the seed.

So the seed itself is already infected before it's even planted.

Precisely.

It's a systemic infection right from the start.

And I remember reading something fascinating about their spore surfaces.

A tiny genetic difference.

Oh yeah, it's pretty neat.

Eue aureae, the covered smut, has smooth tiliospores.

Most other cereal smuts, like the loose smuts, have spiny spores.

And that difference comes down to just two genes.

Incredible.

Just two genes for smooth versus spiny.

Shows how small changes can have visible effects.

Now, regardless of how they germinate, whether budding off spiridia or just fusing hyphae directly, the end goal is always that infectious dichoriotic hypha.

And controlling them.

I assume plant resistance plays a role?

Definitely.

Many cereal smuts have this gene -for -gene relationship with their hosts.

Specific resistance genes in the plant recognize specific avirulence genes in the fungus.

If there's a mismatch, if the plant recognizes the fungus, it triggers a rapid defense, often killing the infected plant cell.

It's called the hypersensitive response.

So breeding -resistant varieties is key.

It's a major strategy.

But the challenge is that the smut fungi are constantly evolving new races that can overcome the plant's resistance genes.

It's an ongoing evolutionary arms race.

Okay, let's switch gears to ustelago made as corn smut.

You said it's a research rock star.

And edible.

Both.

It's probably the most thoroughly studied smut fungus.

It was crucial in early genetics research, like understanding how DNA recombines.

Its haploid yeast phase is super easy to grow and genetically modify in the lab, plus its whole genome is sequenced.

It's become a powerhouse model for studying fundamental eukaryotic biology.

And its lifestyle is different from the cereal smuts.

Quite different in some ways.

Its tiliospores can survive in the soil for years.

And unlike the cereal smuts that often infect seedlings or flowers, Eumates can infect almost any above -ground part of the maize.

Plant leaves, stems, tassels, cobs, usually by entering through natural openings like stomata or even direct penetration.

And it causes those big growths.

Gulls.

Yes, huge gulls, or tumors.

Infected parts swell dramatically, often one to five centimeters across, sometimes much bigger, especially on the ears, the cobs.

This is very different from the small grain smuts, where symptoms are usually restricted to the seeds after that long, hidden phase.

With Eumates, the whole infection cycle, from fusion to new spores, can happen in as little as two weeks.

And this is the part people eat.

Wheat lacosha.

That's the one.

In Mexico, these gulls are considered a delicacy.

While farmers elsewhere might see it as a disease, there it's harvested and cooked.

Tastes kind of earthy.

Mushroomy.

Why does it cause such dramatic swelling?

It's linked to plant hormones.

The fungus itself produces auxins, which are a powerful growth stimulant for plants.

When you analyze the infected tissue, it has much higher levels of these auxins.

So it seems the fungus is manipulating the plant's growth for its own benefit, creating this big, fleshy home full of nutrients.

Bladder fungus.

And you mentioned research using it.

Beyond genetics.

Oh, yeah.

Its mating system, with those A and Bozai, is a classic model.

Researchers have dissected the signaling pathways involved in switching from yeast to hyphal growth, finding key roles for things like KMP and MAP kinases, fundamental signaling molecules in many organisms.

It's also been great for studying the cytoskeleton, how things like microtubules and actin filaments move stuff around inside cells.

And viruses.

Fungi can get viruses.

They can.

Eumates can be infected by mycoviruses, similar to ones found in baker's yeast.

These viruses are basically pieces of double -stranded RNA, and they carry genes for killer toxins.

Killer toxins?

What do they do?

Certain strains of Eumates, if they carry these viruses, will actually kill other compatible Eumates strains when they try to mate.

The toxins attack other fungal cells.

One type, KP4, actually blocks calcium channels, similar to a toxin from black mamba snick venom.

Another might poke holes in membranes.

Wow.

Have people tried to use these toxins?

There have been attempts.

Yeah.

For example, trying to put the gene for the KP4 toxin into wheat to make it resistant to Bunt fungi like Talatia, but there are always public acceptance hurdles with genetically modified crops.

Right.

Speaking of Talatia, the Bunt fungi, you said they're economically important and have a history.

Absolutely.

Around 125 species, all on grasses, Talatia carries, and T -controversial on wheat, T -horida on rice.

These are big deals.

And they cause covered smut symptoms,

like ustelago horidae.

Similar, yes.

The infection is systemic, and the inside of the grain gets replaced by spores, forming those Bunt balls.

But Talatia spores often have this cool net -like surface pattern.

And the smell,

the fishy smell.

Oh, yes.

Trimethylamine.

That's why it's called stinking smut.

Crushed Bunt balls really reek, and it makes the flour totally unusable.

And the history.

You mentioned Prevost and Talate.

Yeah.

Talatia carries is historically significant.

Talate, back in the 1750s, showed the disease was linked to the spores experimentally.

But it was Prevost in 1807 who was crucial.

He saw the spores germinating under his microscope, and realized it was a living organism causing the disease.

A huge conceptual leap back then.

Massive.

And even better, he found that copper sulfate stopped the spores from germinating.

He developed seed treatment with copper sulfate, which was effective chemical control, decades before the more famous Bordeaux mixture was invented for other fungal diseases.

A real pioneer.

So how does Talatia carries actually work, its life cycle?

The Talio spores are tough, surviving up to 15 years.

They germinate with the seed.

Meiosis happens, then mitosis, forming 816 nuclei in the spore.

A promycelium grows out, producing these narrow curved primary sporidia.

With me.

They do, often in pairs, right there on the promycelium, forming characteristic H -shapes.

From that H -shape, a single secondary sporidium develops, and the secondary sporidium is actively shot off.

Shot off.

How?

It uses a surface tension catapult mechanism, like flicking a tiny droplet.

It's this launched secondary sporidium that infects the young seedling shoot, the choleoptile.

Then, systemic growth, no symptoms until the grain heads are nearly ripe.

And you mentioned other Talatia species, dwarf bunt and carnal bunt.

Right.

Talatia controversa causes dwarf bunt.

It likes colder temperatures, so it mainly hits winter wheat, infecting plants under snow cover from spores in the soil.

Causes stunting, hence dwarf.

It became infamous for causing trade disputes, particularly between the U .S.

and China.

And carnal bunt, Talatia indica.

That one's different again.

Named after a city in India, it's often called partial bunt because it usually only infects part of the grain, often leaving the embryo okay.

And it doesn't seem to grow systemically like the others.

Its spores germinate in the soil, produce lots of primary sporidia, then secondary sporidia, which are launched and infect individual flowers on the wheat year later in the season.

Even though it doesn't cause huge yield losses, it still causes major trade headaches because regulations are so strict about its presence.

So these bunts, major problems.

What about the Urocystis group?

The sporeball smuts?

Yeah, Urocystis is defined by its sporeball.

The Tilius spore isn't just one cell, it's one or more dark, fertile cells surrounded by a layer of paler sterile cells.

About 140 species do this.

Any important ones?

Urocystis tritichae causes flag smut, or leaf -stripe smut, on wheat, especially in warmer areas.

The fertile cell germinates, makes a promycelium, then primary sporidia that conjugate.

The resulting infection hypha penetrates the seedling, grows systemically, and symptoms those stripe -like sori on the leaves appear much later after flowering.

Okay, we've seen the problems they cause.

How do we actually control these smut and bud diseases?

Well, the strategy depends heavily on whether it's a covered smut or a loose smut because of how they infect.

Covered smuts, where spores are just on the seed surface, were easier historically.

Like Prevost's copper sulfate treatment.

Exactly.

That worked well.

But loose smuts, with the fungus already inside the embryo, that was tough.

The breakthrough came from Jens Ludwig Jensen in Denmark in the 1880s.

The hot water treatment.

That's the one.

He figured out the smut fungus was less heat -tolerant than the cereal grain.

So you could soak infected seeds in cold water, then give them a carefully controlled dip in hot water, like 54 degrees C for wheat, 52 degrees C for barley, long enough to kill the fungus inside but not harm the seed embryo.

Pretty ingenious for the time.

Clever.

What about modern methods?

Now we have very effective systemic fungicidal seed dressings, often a mix of fungicides that penetrate the seed and protectants that stay on the surface.

These handle both loose and covered smuts, and often other seed -borne diseases too.

And preventing infection in the first place.

Seed certification is key for loose smuts.

Since infection happens at flowering, fields grown for seed production are inspected.

If they find too many smutted plants, the seed from that field can't be certified.

We can also now directly test seed embryos for hidden infections using microscopes, or much faster and more sensitively, with PCR -based DNA tests.

Like a diagnostic test recie - That's exactly.

These PCR methods are getting really sophisticated, used for checking grain quality, disease surveillance, even potentially detecting bioterrorism threats using plant pathogens.

And of course, if infection does happen in the field, some systemic fungicides sprayed on the growing crop can suppress smuts, often as a side benefit when treating other diseases.

And plant resistance.

Still important.

Hugely.

Breeding resistant crop varieties using those gene -for -gene interactions is still a cornerstone of control.

Though, interestingly, despite ustelago medes being such a well -studied model organism with its genome sequenced, we actually know surprisingly little about the specific mechanisms of resistance against it in corn.

A bit of a puzzle, still.

Okay, so that covers the true smuts and bunts.

But you mentioned relatives that break the rules.

Or even imposters.

Yeah, this is where fungal taxonomy gets fun.

There's an order called the microbotrials.

These fungi cause diseases that look exactly like smuts, telospores, promycelium, yeast phase, infectious decarion… the whole package.

But they aren't actually ustelaginomycetes.

Nope.

Molecular studies looking at their DNA clearly place them in the uridinomycetes.

They're actually rust fungi that have convergently evolved a smut -like lifestyle.

Wow, evolution playing tricks on us.

How can we tell them apart, then?

Subtle microscopic things.

Their growth inside the plant is strictly between cells intercellular, whereas many true smuts grow intracellularly.

And their telospores often have a distinct violet or purplish tinge, not the typical brown of true smuts.

Let's talk about one of those microbotrium -violaceum, the anther smut.

It sounds like it does some crazy stuff to its host.

It really does.

It infects plants in the carnation family, like campions.

The fungus grows systemically, all through the plant, but the symptoms only show up in the anthers, the pollen -producing parts of the flower.

Instead of pollen, they get filled with purple telospores.

Okay, but the really wild part?

Does sex change?

Right.

On host plants that have separate male and female flowers, like white campion,

if a female plant gets infected, the fungus makes it produce anthers.

It chemically tricks the female flower into developing male parts.

Why would you do that?

To spread its spores.

It needs pollinators to visit the anthers to pick up spores and carry them to the next flower, so it ensures even female plants have spore -filled anthers for the insects to visit.

It's thought to involve a fungal signal that mimics the plant's male -determining Y chromosome.

That is mind -blowing manipulation.

It's essentially a sexually transmitted disease for plants spread by pollinators.

You got it.

And studying how its yeast cells fuse led to a major discovery in fungal biology, Fimbria.

Fimbria, like little hairs.

Exactly.

Tiny, hair -like appendages on the yeast cells that help compatible mating types stick together initially.

And the protein making up these Fimbria, it turned out to be incredibly similar to collagen.

Collagen, like in our skin and bones.

Found in a fungus.

Yes, a huge surprise at the time, thought to be an animal -only protein.

It shows how much we're still learning.

These Fimbria also have specific sugars involved in recognizing the right mating partner, and even bits of RNA whose function we don't fully understand yet.

And ecologically, this anthrosmite has other effects.

Oh yeah.

Infected plants might flower earlier, manipulating pollinators.

The disease can reduce the plant's root system, affecting its ability to survive winter.

And hosts can adapt too, maybe by making smaller flowers or switching to an annual lifestyle to ditch the overwintering fungus.

It's a complex ecological dance.

Okay, so we've had true smuts, rest imposters.

What about the last group, the Exobasidiales?

Still Estilogenomycetes, but different.

Right, the Exobasidiales are definitely Eustilogenomyces, but they break some key smut rules.

They're still obligate plant pathogens, less than 100 species, with that typical yeast phase and infectious dicaryotic phase.

But what's different?

Big difference, number one.

No thyliospores.

They don't make those thick -walled rusting spores.

Instead, their Basidia, the structures that make the sexual spores, form directly on the surface of the infected host plant.

And the Basidia themselves look different.

They look simpler, more like the club -shaped Basidia you see in mushrooms, Homo Basidiomyces.

But developmental studies show nuclear fusion happens in a cell below the Basidium, so technically it's still equivalent to the smut and rust system, just looks different.

Interesting.

Other differences.

Their Basidiospores are shot off forcefully using that same surface tension catapult we saw in Tulasia, and they often become septate -developed internal walls after they're discharged.

Also, their mycelium inside the plant is usually intercellular between cells, and they often do form hostoria, but these look different from rust hostoria and aren't usually surrounded by that full sheath, like in smuts.

They form a more complex interaction apparatus at the tip.

Let's use exobasidium itself as the example.

What does it do?

There are about 50 species.

They cause local leaf infections or sometimes infect hole shoots.

A classic symptom is hypertrophy.

The infected tissue swells up, often looks pale or reddish.

Clearly there's a hormonal mess -up happening in the plant.

What kinds of plants do they infect?

Very commonly plants in the Heather family, the Erychaceae, think Faxinium species, blueberries, bilberries, also azaleas, and rhododendrons often get hit.

Another big one is the tea plant, Camellia sinensis.

Exobasidium vexans causes a disease that really hurts tea harvests, affecting both quantity and quality.

And their life cycle, briefly.

Eventually you see this whitish layer of basidia on the surface of the swollen plant tissue.

Each basidium makes maybe two to eight spores.

These spores are shot off, might become septate, and can germinate to form germ tubes or those elongated yeast cells.

They can overwinter inside the host plant systemically, or maybe as spores hiding in buds or on bark.

Wow.

Okay, we've covered a lot of ground.

From true smuts and bunts to imposters to these rule breakers, what's the big picture takeaway here?

I think it's the incredible precision and diversity of these fungi.

They use really specific biological tools, pheromones for mating, unique structures for feeding, manipulating host hormones, even using physics for spore dispersal.

They're masters of adapting their life cycle to exploit specific plant hosts.

And we've seen their huge impact, right?

Shaving agriculture, driving trade policies for centuries, even ending up as food.

Plus, the fundamental biology we learn from studying them is invaluable.

Absolutely.

The sheer variety, true smuts, the rusts acting like smuts, the ex of the basidials doing their own thing.

It just highlights this incredibly complex dynamic relationship constantly playing out between fungi and plants.

It's a fantastic window into evolution and ecology.

It really is a reminder that there's just immense complexity and ongoing discovery happening in the microscopic world, things that have massive effects on our own lives.

And you know, there's always more to uncover.

We've only scratched the surface of what these organisms are capable of.

Endlessly fascinating.

Well, thank you for joining us on this deep dive into the world of smut fungi and their allies.

We hope you picked up some surprising facts and feel a bit more clued into these amazing fungal transformers.

Keep asking questions, keep exploring, and we'll catch you on the next deep dive.