Chapter 15: Hymenoascomycetes: Helotiales (inoperculate discomycetes)

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What if I told you there's like an entire hidden kingdom of organisms,

you know, quietly shaping our world, influencing everything from the food we eat to even the air we breathe.

Often totally unseen, but really impactful.

It's kind of amazing when you think about it.

Yeah.

So welcome to the deep dive.

We take complex topics, break them down.

And today we're plunging into a really fascinating corner of the fungal kingdom.

It's a group called the helotials.

That's right.

We're digging into chapter 15 of introduction to fungi, focusing on these guys, specifically the inoperculate dyskamecetes.

Sounds technical, I know.

It does sound a bit technical, yeah.

But our mission today is basically to unpack all that dense science.

We're talking morphology, life cycles, ecology, what these fungi actually do in the world.

And importantly, make it clear and engaging without any pictures, just audio.

Exactly.

Think of it as your shortcut to get included on a pretty surprising group of organisms.

So what makes these helotials stand out right away?

Well, the key thing lies in something quite specific, how they release their spores.

Most fungi, you know, they have the spore producing sac called an ascus.

Sometimes it has a little lid or an operculum that pops open.

Right.

I can picture that.

But not the helotials.

They're assy.

They often have two layers making them betunicate.

But they release spores not through that detachable lid, but through more of a like a valve or a tiny slit.

Oh, interesting.

So more like a subtle pressure release, not a pop top can.

Exactly.

And the fascinating bit is even with those two layers, the layers stay together during spore release.

They're non -fissitunicate.

It might sound like jargon.

A little bit.

Yeah.

But it's actually a key identifier for this group, a kind of fungal fingerprint.

OK, so that's a defining feature.

Let's unpack the sheer diversity then.

You mentioned it's a big group.

Oh, it's massive.

The helotials order contains an estimated 2300 species.

2300.

Wow.

Yeah.

And despite being so common, classifying them can be, well, a real puzzle, even for scientists.

There's debate about whether the order is truly monophyletic, you know, all descended from one common ancestor.

So even the experts are still figuring parts out.

That tells you something about how complex fungi are.

It really does.

Fungal taxonomy is always evolving.

But what we do know is how incredibly adaptable they are.

They've mastered so many different ecological situations.

Right.

You see them everywhere doing different things.

Absolutely.

You'll find many as significant plant pathogens.

They cause diseases that can, you know, devastate important crops.

How do they do it?

Different ways.

Some are necrotrophic.

They kill the host tissue first, then feed on the dead stuff.

OK.

Others are biotrophic, living on living tissue without killing it right away.

And some are hemibiotrophic.

They start one way, maybe biotrophic, then switch to necrotrophic.

So they can be destroyers, but also recyclers.

That's amazing versatility.

And it goes further.

Many are saprotrophs.

They're crucial decomposers, breaking down dead leaves, woody plants, all that organic matter.

OK, the cleanup crew.

Exactly.

But here's a cool twist.

Some also live totally harmlessly inside living plants as endophytes.

Inside the plant.

Yeah.

Without hurting it.

Yeah.

And it's actually suspected that many fungi we normally think of as decomposers might start their lives this way, just hanging out inside the plant until it dies.

Huh.

That changes how you think about them.

It does.

We also see them in freshwater streams, making weirdly shaped spores to cope.

And they form vital partnerships, aricoid mycorhizal associations with plants like heather and blueberries, helping them get nutrients.

So they help plants, too.

And then you've even got some groups,

the Phthalobalaceae, that thrive on dung.

They're coprophilous.

OK.

From crop killers to dung dwellers to plant helpers.

That's a seriously wide range of lifestyles.

Let's zoom in on some of the really impactful ones, maybe the plant pathogens first.

The Sclerotinaceae family sounds important.

It really is.

Sclerotinaceae and their close relatives, the Rastromaceae, they share a key feature.

They produce these cup -shaped fruiting bodies.

The apothecia you mentioned.

That's them, yeah.

Apothecia.

And they grow from these special food storage organs called stromata.

Stromata?

Like a pantry.

Exactly like a pantry.

Or maybe a survival bunker.

It lets the fungus overwinter inside the host plant tissue and then pop out with its apothecia in the spring.

Clever.

And are these stromata all the same?

No.

There are basically two main types.

You've got the Sclerotial stroma, or just Sclerotium, that was pretty distinct, like a little nugget.

OK.

Imagine a dark, thick -walled outside, like a rind, and a core of clear fungal cells inside.

It's made purely of fungal hyphae, fungal threads, and it's typical of the Sclerotiniaeaceae.

Got it.

And the other type.

That's the substratal stroma.

It's much less obvious, more like a diffuse network of fungal threads that permeates the host plant material itself, kind of preserving it while feeding on it.

That's more common in the Rastormaeaceae.

It's fascinating how that subtle difference in their storage strategy helps classify them.

And these fungi, they're super flexible in how they reproduce asexually too, right?

What's the deal with their spores, or knidia?

Yeah, their reproductive flexibility is a huge advantage.

Many produce macroknidia.

These are usually larger spores, they germinate easily, and they're great for spreading disease quickly.

Big spores for quick spread.

Makes sense.

But then they often also have microknidia.

These are smaller, might not germinate as readily on their own.

So what are they for?

Well, they're primarily thought to function as spermatia.

Basically they act like little fertilizing agents in sexual reproduction.

So they help mix up the genes.

Exactly.

This dual strategy is key.

They can rapidly colonize with macroknidia, or they can use microknidia for sex, increasing genetic diversity.

That's crucial for adapting, you know, developing resistance, stuff like that.

A toolkit for both invasion and evolution.

Can you give us some examples?

How does this play out with specific fungi?

Sure.

Let's take Sclerotinia monolinia fructigena.

That's the one causing brown fruit rot in apples, pears, plums.

Big problem.

Yeah, I've seen that.

Nasty stuff.

It produces chains of blastoconidia that's a type of macroconidia that spread the disease really effectively.

But it doesn't bother making microconidia.

Okay, so it's all about the rapid asexual spread.

Pretty much.

Then you have Sclerotinia sclerotiorum, a major, major pathogen we'll talk more about.

It actually skips the microconidia.

It only makes microconidia, likely just as spermatia for its sexual cycle.

Huh.

Completely different strategy.

Right.

And then there's Sclerotium cipivorum.

This causes white rot in onions and garlic.

It's a real outlier.

How so?

What makes it weird?

Well, it produces neither functional conidia nor apathasia.

It's sclerotia, those little survival bunkers, they just act as vegetative propagules.

They spread just by growing fungal threads outwards.

So it doesn't really do spores at all.

Nope.

Its connection to the Sclerotinacea was actually a surprise, only confirmed by DNA studies.

Shows you can't always judge a fungus by its cover.

Definitely not.

Okay, let's talk damage and control, especially for the ones hitting our crops, like that Sclerotinia sclerotiorum you mentioned.

Sounds like a big deal.

It's a huge deal.

Causes things like Sclerotinia rot, white mold, stock break, affects over 400 plant species.

400?

Yeah, including really vital crops, sunflowers, soybean, oilseed rape, canola.

In bad years, it can cause almost 100 % crop loss.

That's devastating.

And you said its sclerotia will last for years in the soil.

Three years.

Makes it incredibly hard to get rid of once it's established.

So how does it actually infect plants and cause so much trouble?

What's its secret?

It's got this complex sort of three -phase life cycle.

First, it acts like a decomposer, a saprotroph growing on dead stuff like fallen leaves or petals.

Okay.

Puts up its biomass.

Okay, gets its strength up.

Then, wham, it launches a necrotrophic attack on the living plant tissue, killing it really fast.

The killer phase.

Right.

And then once the tissue is dead, it goes back to being a saprotroph, feeding on the remains and crucially, forming lots of new sclerotia to survive until the next opportunity.

A vicious cycle.

What's its weapon then?

How does it kill so fast?

Its main weapon is oxalic acid.

Eschlorosium pumps out large amounts of this stuff into the plant tissue it infects.

Oxalic acid?

Isn't that in rhubarb leaves?

It is, yeah.

But here, it's not just a toxin.

It's like a multi -tool for the fungus.

It binds up calcium ions in the plant cell walls.

Why is that important?

Well, calcium is important for plant cell structure and signaling.

By removing it, the fungus weakens the plant.

It also suppresses the plant's own defense response, something called the hypersensitive response, where the plant tries to kill cells around an infection point to stop it spreading.

So it disarms the plant's defenses.

Clever.

Very.

And maybe, most importantly, the oxalic acid makes the surrounding tissue acidic.

Really acidic.

And why does the fungus want that?

Because that acidic environment is absolutely perfect for its other weapons.

Its pectin -degrading enzymes, things like endopolytic electronuses.

These enzymes literally dissolve the glue holding plant cells together, the pectin.

Wow.

So it creates the perfect acidic soup to dissolve the plant from within.

That's a pretty good description.

It macerates the tissues, breaks them down, leading to that typical soft, watery, raw in the white mold look.

And the fungus is smart.

It can even sense the pH and tweak its oxalic acid production accordingly.

That's incredibly sophisticated for a fungus.

How on earth do farmers control something like that?

It is really challenging.

Sometimes esclerosiorum can be seed -borne.

It actually survives inside the seed embryo.

But often, fungicidal seed treatments can handle that.

Okay, so treating the seeds helps.

What about infections already in the field?

That's tougher.

But biological control is looking really promising.

There's another fungus called coniotherium minitans.

A fungus fighting a fungus.

Exactly.

Coniotherium is a parasite of sclerotinia esclerosiorum's sclerotia.

It attacks and destroys those survival bunkers in the soil.

So you introduce the good fungus to kill the bad fungus' dormant stage.

Precisely.

It essentially decontaminates the soil.

It works so well, it's actually registered and sold as a commercial biocontrol agent in some places.

That's fantastic.

Nature's solution?

Any other approaches?

Yeah.

Looking ahead, research is exploring transgenic crops.

They've put an oxalate oxidase gene from cereals like wheat or barley into susceptible plants like soybeans.

This enzyme breaks down oxalic acid.

Ah, so the plant fights back by neutralizing the fungus' main weapon.

That's the idea.

And those plants show pretty good resistance.

Conventional breeding for tolerance to oxalic acid is also ongoing.

Fascinating stuff.

Now, what about that other tricky one?

Sclerotium sepivorum, the onion and garlic white rot.

You said its sclerotia lasts for decades.

Decades, yeah.

It can make fields basically unusable for growing onions or garlic.

A real nightmare for growers.

So how do you deal with something that persistent?

You can't just wait it out.

No, you can't.

But here's where understanding the biology leads to a really clever control strategy.

It turns out the sclerotia don't just germinate randomly.

They need a trigger.

A trigger.

What kind of trigger?

Chemicals released by the roots of allium plants.

Onions, garlic, leeks.

Things like alkylcysteine sulfoxides.

These chemicals signal to the sclerotia, hey, food's here.

Time to wake up.

Okay.

So how do you use that?

You trick them.

You can spray chemicals onto the infested soil that mimic these root signals.

A common one is diolid desulfide.

That's actually a major flavor component of garlic itself.

You spray garlic smell on the field.

Basically, yes.

Or similar compounds.

This tricks the sclerotia into germinating when there are no actual host plants around.

And without a host.

They've got nothing to infect, no food source, so they just die.

It's called suicidal germination.

You essentially trick the fungus into exhausting itself.

Some studies show even just working garlic powder into the soil can have a similar effect.

That is brilliantly sneaky, using the fungus' own cues against it.

It's a great example of targeted control based on ecological understanding.

And again, biological control is also being looked at using trichoderma fungi that produce enzymes to break down the S -sepivorm hyphae.

Lots of different angles.

Okay, let's move on to probably the most famous or infamous one.

Botryatina faecaliana, or as most people know it, Botrytis Scenaria.

Grey mold.

Ah, yes.

Grey mold.

Ubiquitous.

While at sexual stage, Botryatina faecaliana with the apetitia is pretty rare to see.

We mostly see the asexual form.

Exactly.

Botrytis Scenaria.

It causes grey mold on just a huge range of plants.

Fruits, vegetables, flowers, even conifers sometimes.

And it's important to remember, Botrytis Scenaria isn't just one thing.

It's really a complex, a collection of several genetically distinct strains.

Right now, it causes massive crop losses, obviously.

But then there's this completely different side to it.

The noble rot in wine grapes.

How does that work?

How can the same fungus be both terrible and amazing?

Isn't that fascinating?

It really highlights how context is everything in biology.

Normally, yes, Botrytis causes severe bunch rot in grapes.

The berries get covered in mold, shrivel up into these useless mummies, huge losses for The destructive side.

But UT, under very specific conditions, the right climate,

misty mornings, sunny afternoons, the right timing, and crucially, the right grape varieties, like Sémillon or Riesling.

The infection proceeds differently.

It becomes noble rot, or pour tour noble in French.

The fungus gently penetrates the grape skin, allowing water to evaporate without the berry just rotting away completely.

So it dries the grape out, concentrating everything else.

Precisely.

It concentrates the sugars, the acids, the flavors.

The grapes shrivel, yes, but in a good way.

This process is absolutely essential for making some of the world's most prized sweet berserk wines.

Like, so turns.

Wow.

So the winemaker is actually managing a fungal infection to create a luxury product.

They are.

It's a delicate balance.

Too much moisture, you get gray mold disaster, just right where you get liquid gold.

It really shows the fine line.

That's a perfect aha moment for our listeners, I think.

So when it is being destructive, causing all that gray mold, how does it actually attack the plant?

What's the strategy?

Well, B Scenaria is considered a classical mechatrophic pathogen.

Like Sclerotinia sclerosiorum, its main game is to kill host tissue rapidly, then live off the dead remains.

Okay, kill first, eat later.

What tools does it use?

They have a whole arsenal.

First, attachment.

The spores, the macrocanadia, have a hydrophobic surface, kind of water repelling, which helps them make initial contact.

Weak attachment at first.

Just sticks lightly.

Yeah.

But then, when the germ tube starts to grow out of the spore, it secretes this sticky matrix.

It's polysaccharide -based, contains stuff like Scenarian, which is a type of glue can.

What does the matrix do?

It's like biological superglue.

It anchors the fungus firmly to the plant surface, but it's also thought to be a carbohydrate reserve, like a packed lunch for the fungus, and it acts as a platform to hold its enzymes close to the plant surface.

Lose itself down and brings its weapons.

What are the weapons?

Lytic enzymes.

Lots of them.

Enzymes that break things down.

Cutin -degrading enzymes to get through the plant's waxy cuticle, proteins to break down proteins, and especially pectinolytic enzymes.

Ah, the pectin dissolvers again.

Like Sclerotinia.

Exactly.

Pectin is a major component of the plant cell wall middle amella, the stuff holding cells together.

Breaking it down causes widespread tissue maceration, that soft mushy rot characteristic of gray mold.

And guess what else helps?

Let me guess.

Oxalic acid.

You got it.

Oxalic acid again, creating that acidic environment perfect for the pectin enzymes and messing with the plant's calcium.

It's a recurring theme, this acid attack.

But surely the plant fights back.

You mentioned the hypersensitive response before.

It does fight back.

The plant triggers that hypersensitive response programmed cell death around the infection site.

Often involves an oxidative burst, producing reactive oxygen species, and the production of phytoalexins, which are antimicrobial compounds.

So the plant tries to sacrifice cells to contain the invader.

Does it work against Botrytis?

Here's the really insidious part.

While that defense works well against many pathogens, especially biotrophs, Botrytis, being a necrotroph, actually exploits those dead cells the plant creates.

Exploits them?

How?

It uses them as an easy source of nutrients to get established.

And it's armed against the plant's chemical weapons, too.

It produces enzymes like superoxide dismutase and catalase to neutralize the reactive oxygen, and other enzymes like lacase to detoxify the phytoalexins.

It even has special pumps, ABC transporters, to actively pump out any plant toxins that get inside its cells.

Wow.

So the plant's attempt to defend itself can actually help the fungus get started.

In some ways, yes.

It's a remarkable example of counter -adaptation.

The host's defense facilitates the infection by the necrotroph.

That is just mind -blowing.

No wonder it's so hard to control.

Fungicides must struggle.

It's a massive problem.

Botrytis' scenario has developed resistance to pretty much every class of fungicide currently used against it.

Why is it so good at becoming resistant?

Several reasons.

Its ability to reproduce sexually means it's constantly shuffling its genes, creating new combinations, some of which might confer resistance.

The fact that it exists as multiple distinct genetic strains means there's already a lot of variation out there.

Plus it has things like mobile genetic elements, bits of DNA that can jump around the genome and potentially spread resistance genes quickly.

So it's genetically diverse and adaptable.

How does the resistance actually work at the cellular level?

Various mechanisms.

Sometimes the fungus changes its cell wall or membrane so less fungicide gets in.

Sometimes it ramps up those efflux pumps, the ABC transporters, to pump the fungicide back out faster.

Sometimes it produces enzymes that chemically modify and detoxify the fungicide.

And sometimes the target protein that the fungicide is designed to inhibit mutates so the fungicide doesn't bind properly anymore.

It's a constant arms race.

A very challenging arms race for agriculture.

Okay, let's shift gears a bit.

What about the Dermatisi family?

You said they were small and inconspicuous.

Yeah, relatively speaking.

Taxonomists think this family is probably polyphaletic, meaning the members don't all share a single recent common ancestor, so it's likely to be revised.

Their apathecia, the fruiting bodies, are tiny, usually under a millimeter across.

Tiny cups.

Right.

And they grow directly on the substrate, like dead wood or plant stems, without forming those big stroma structures we saw earlier.

They also have this interesting development pattern called hemiangeocarpic.

Hemiangeocarpic.

Right, you mentioned that.

Can you paint that picture again?

How does it work?

Okay, imagine the fungus starts by forming a tiny, closed, almost spherical structure inside the plant tissue or on the surface.

It looks a bit like a tiny sclerotium or maybe a clastothesium, a completely closed fruiting body.

It's protected.

Okay, like a little hidden ball.

Exactly.

Then, a pore, a little opening, develops right at the apex, the top.

And this pore then expands sideways, opening up the structure into that flat, disc -like apathecium, often with a distinct rim or margin.

It's like it unfolds from the inside out.

That's neat.

A protected start, then opening up.

What do these guys do ecologically?

A mix as usual with phylicials.

Many, like a common one called Malesia Scenaria, are saprotrophs, decomposing dead wood.

Others are hemibiotrophic plant pathogens.

They cause diseases, but often more limited lesions compared to, say, sclerotinia.

Any examples that cause significant crop problems?

Yes, a couple are quite important.

Pyranopiziza brassicae causes light -leaf spot on winter oilseed rape, that's canola again.

Big problem in some areas.

And then you have the Tapezia species.

Tapezia yellandae is a major cause of eye -spot disease at the base of cereal stems, particularly winter wheat.

There's a sister species, T.

aciformis, that does the same thing on rye.

Eye -spot.

Does that weaken the stem?

It does.

It creates these characteristic grayish -brown, eye -shaped lesions near the soil line.

This can weaken the stem, making the crop prone to lodging falling over, and it can also restrict nutrient flow, affecting grain development.

How does it infect the plant?

Infection is mainly by these needle -shaped knidia, the asexual spores, which get splashed around by rain from old, infected stubble left over from the previous harvest.

The ascospores, the sexual spores, can also infect, though.

When a spore lands on the stem base, it forms what's called an infection plaque, basically a little mat of fungal hyphae.

Okay, so that's a base camp.

Pretty much.

From this plaque, numerous specialized infection structures called a presoria form.

These are often melanized, darkened, and tough.

They build up kerger pressure, like inflating a tiny balloon against the plant surface, and also secrete enzymes to punch their way through the cuticle and cell wall.

Pressure and enzymes.

The classic fungal -breaking tools.

Exactly.

And once inside, it causes that eye spot lesion.

And like with protritus, fungicide resistance is becoming an issue for controlling Tapegia eye spot, too.

Seems to be a recurring theme with these successful pathogens.

Okay.

Alright, let's move on again to the Ritismataceae family.

This includes the famous tar spot fungus, right?

That's the one.

Ritismataceae.

Again, the taxonomy of this whole family is a bit messy, likely polyphaletic.

But generally, their apothecia are either immersed within the host tissue or within flat, crust -like stromata.

They often have a mechanism where the covering layer splits or cracks open to reveal the hymenium, the actual spore -producing layer underneath.

And where do you find these?

Mostly associated with trees, either broadleaf trees or conifers.

And ecologically, it's the familiar spectrum.

Some are endophytes living harmlessly inside, some are saprotrophs on dead material, and some are quite severe pathogens.

There's evidence suggesting some of the pathogens actually evolved from endophytic ancestors.

Interesting evolutionary path.

So tell us about Ritismataceae, the tar spot.

I think many people will have seen this on sycamore or maple leaves.

Very likely.

It's extremely common.

Forms those very distinctive black, shiny, slightly raised spots on the upper surface of sycamore leaves, usually about one or two centimeters across.

Looks just like drops of tar.

It really does.

How does it develop?

The infection actually happens in the spring, but the symptoms first appear as yellowish spots on the leaves during the summer.

These gradually enlarge and turn black as the fungal mycelium develops extensively within the leaf tissue, forming that stroma.

Does it have an asexual stage?

It does.

Within those black tar spots, it forms a cannidial state called melasmia acerina.

This produces these little flask -shaped cavities, sometimes called spermogonia, which release masses of tiny, curved, spore -like structures.

Those for spreading the disease?

Interestingly, no.

These are thought to be Spermatia microcanadia again that don't actually germinate to cause new infections, but are believed to be involved in fertilizing the fungus for its sexual stage.

Ah, the sexual function again.

So the main event happens later.

Yes.

The apothecia, the sexual fruiting bodies, develop within those black stroma, but only after the leaves have fallen in the autumn.

They mature over the winter on the fallen leaves, ready for the spring.

And how do the spores get out of those tar spots on the dead leaves?

By spring, typically March or April, cracks appear in the surface of the black stroma, exposing the hymenium underneath.

And then the asco spores are discharged, often quite dramatically, by puffing.

Puffing?

Yeah, you can sometimes see a little cloud of spores being released if you disturb infected leaves at the right time.

The spores themselves are quite large, needle -shaped, and they get actively shot out, maybe about a millimeter.

Just a tiny jump.

Just a tiny jump initially, but enough to get them into air currents, which then carry them up to the newly emerging sycamore leaves.

How do they stick to the new leaves?

They have a sticky mucilaginous epospore, a slimy outer layer that helps them adhere.

They typically land on and infect the lower surface of the leaf, entering through the stomata, those tiny pores the leaf uses for gas exchange.

A very well -defined life cycle.

And this fungus has that amazing connection to air pollution, right?

This is the really cool part, ecologically.

It turns out that Redisma acerenum is very sensitive to sulfur dioxide pollution in the air.

Sulfur dioxide, like from burning coal?

Exactly.

High levels of SO2 inhibit the germination of its asco spores.

So in areas with heavy industrial pollution, historically you just wouldn't find tar spot, even if sycamore trees were plentiful.

So its presence or absence tells you something about the air quality?

Precisely.

It became recognized as a bio -indicator.

The presence and abundance of tar spot on sycamore leaves can be used as a rough visual index of local air pollution levels, specifically for sulfur dioxide.

If you see lots of tar spot, the air is likely relatively clean, at least of SO2.

That is absolutely fascinating.

A fungus acting as a natural pollution monitor right on the trees around us.

Okay, we've covered some major groups, but you mentioned other helo -shells too.

Some hidden gems, maybe brightly colored ones.

Oh yes, there's still more variety.

Many helo -shells are quite striking.

Think about the geoglossaceae.

The earth tongues.

Earth tongues.

What do they look like?

They form these quite conspicuous club -shaped or tongue -shaped fruiting bodies, usually dark -colored, growing directly out of the ground.

They're saprotrophic, decomposing organic matter in soil.

Any specific examples?

A good one is Trachoglossum hirsutum, the hairy earth tongue.

It's black, often flattened, can be up to maybe 8 cm tall.

And you find it in grassy areas, pastures, lawns.

It's distinctive because its surface is covered with these black, thick -walled bristles called hymenial sea -tie mixed in among the acai.

Hairy earth tongues.

Okay.

How do they shoot their spores?

You mentioned they have long spores.

They do have very elongated ascus spores.

And their discharge is quite remarkable.

The ascus tip bursts, but only a tiny pore opens.

One spore at a time squeezes through this pore.

As it exits, it temporarily blocks the pore.

Like a valve?

Sort of, yeah.

Pressure builds up behind it, then that spore gets ejected quite rapidly.

The next spore immediately moves into the pore, blocks it, pressure builds, pop, it goes.

This happens sequentially, one after the other, single file, until all 8 spores are discharged.

That is incredibly precise.

A little spore machine gun.

It's a very neat mechanism.

Then you have groups like the leocese.

Small group, separatrophic again, but known for brightly colored fruit bodies.

Leocese lubrica is famous, people call them jelly babies.

Jelly babies?

Yeah, they look like little gelatinous yellowish green or olive green blobs with a stalk found in woodland humus.

Quite charming.

I'll have to look out for those.

What about the helocese themselves?

That sounds like a core group.

It's a huge family, probably the largest within the order, and almost certainly polyphaletic, needing a lot more taxonomic work.

It includes all sorts of things.

Genera like ascocorine and neobulgaria form sort of gelatinous, often pinkish or purplish apothecia on dead wood.

And then there's chlorociboria.

This one is amazing.

It produces these beautiful small cup -shaped apothecia that are a stunning turquoise green color.

Bright green.

Intense green.

But the really cool thing is the fungus' mycelium stains the wood.

It grows in that same vibrant green color.

It dyes the wood green.

Permanently.

This green oak or green -stained wood was highly prized historically, especially in the Renaissance, for use in decorative woodwork, marquetry, things like tunbridge ware, using a fungus as a natural wood stain.

That is incredible.

A woodworking fungus.

Yeah.

You also mentioned mycorrhizal associations earlier with the heather -type plants.

Yes.

That's another crucial role played by some helocellists, particularly within this broad holoshishi group.

The classic example is Hymenosophus erikei.

It forms what's called ericoid mycorrhiza.

Erecoid.

For erikishi plants.

Like heather, rhododendrons, blueberries.

Exactly those.

These plants typically grow in really poor acidic soils, like heathlands and peat bogs, where nutrients, especially nitrogen and phosphorus, are hard to come by.

They also have very fine, delicate root systems called hair roots.

Okay.

Hymenosophus erikei infects the epidermal cells, the outermost layer of these hair roots.

It doesn't kill the cells.

Instead, it grows inside them, invaginating the plant cell membrane, pushing it inwards, and forming dense, hyphal coils within the cell.

A coil of fungus inside the root cell.

What's the benefit?

It's a symbiosis, a partnership.

The fungus is much better at scavenging scarce nutrients, particularly organic forms of nitrogen and phosphorus from the acidic soil, than the plant root is on its own.

The fungus absorbs these nutrients and transfers them to the plant.

In return, the fungus gets sugars, carbohydrates from the plant's photosynthesis.

So the fungus feeds the plant nutrients from poor soil, and the plant feeds the fungus sugars.

A classic mycorrhizal deal.

Precisely.

This ericoid mycorrhizal association is absolutely vital for the survival and success of these ericaceous plants in those challenging environments.

A hidden partnership driving entire ecosystems.

Any other weird and wonderful groups?

Oh, there's the bulgariaceae.

Bulgaria inquinons is a common one, forms large, black, gelatinous, sort of top -shaped apothecia on recently felled oak and beech trees.

Looks a bit like black jelly drops.

Okay.

Anything special about it?

One unusual thing is that when its asphysts matures, it contains a mix of spores.

Typically four are dark brown, melanized, and four remain clear, hyaline, all within the same sac.

The reason for this isn't fully clear, and it might even live as an endophyte inside the tree before it's felled.

Fascinating mix of spores.

And finally, maybe the most unusual,

the cetariaceae.

Ah, yes, cetaria.

These are really something else.

Definitely some of the most bizarre helociales.

They are biotrophic parasites, meaning they live on living hosts, specifically on southern beech trees,

nauthofagus.

Another beech.

So not around here in the northern hemisphere?

No.

You find these in places like South America, Chile, Argentina,

and also Australia and New Zealand, wherever nauthofagus trees grow.

What do they look like?

They cause the tree to form these woody growths called galls on its branches.

And then growing out of these galls are the fungal fruiting structures.

They're these amazing spherical or pear -shaped apothecial stromata.

Imagine an orange or pale yellow dimpled ball, maybe the size of a golf ball or even larger, hanging off the branch.

A ball of dimples.

Yeah.

And each one of those dimples on the surface is actually a single embedded apothecium.

The whole structure is a compound fruiting body made of many apothecia packed together in a fleshy stroma.

That sounds incredible.

Do they release spores?

Oh, yes.

They release huge numbers of dark -colored asco spores.

And interestingly, the fleshy stromata of some Ceteria species are actually edible.

They're harvested and eaten by indigenous peoples in South America, sometimes called Indian bread.

Edible fungal galls.

That's definitely unique.

What a journey through this group.

It really shows the incredible diversity packed into just one order of fungi, doesn't it?

From microscopic spore details to ecosystem -level impacts.

Absolutely.

We've gone from their unique spore release, that inoperculate non -physitunicate thing, through their amazing ecological range.

Devastating pathogens like Sclerotinia and Botrytis, essential decomposers, vital mycorrhizal partners like Hymenosophus, weird forms like Earth tongues and Ceteria, even influencing air quality monitoring and creating noble rot for dessert wines.

It's a perfect illustration of how these inoperculate dyskomyces, as the chapter calls them, are true masters of adaptation.

Flexible life cycles, complex chemical interactions with their hosts and environment.

They really shape our world in profound ways, often completely unseen.

So what's a big takeaway for you listening?

I think it's that this intricate world of fungi, groups like the hilloshales, really reminds us that even the smallest, seemingly hidden organisms wield immense power.

They play absolute critical roles in the balance of life on Earth.

Makes you wonder, doesn't it?

It really does.

What other hidden biological processes, maybe fungal, maybe something else entirely,

are silently influencing our lives, our planet, right now?

Just waiting for us to notice and uncover their secrets.

Something to think about.