Chapter 9: Archiascomycetes

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Okay, let's unpack this.

When you think of fungi, what first comes to mind?

Probably mushrooms, right?

Or maybe mold.

Yeah.

Or even the yeast in your bread.

Sure.

Common examples.

But today, we're taking a deep dive into a group that might challenge everything you thought you knew about the fungal kingdom.

We're talking about the archaeascomyces.

Yeah, and what's fascinating here, this isn't just about obscure organisms.

It's really about peeling back the layers of evolutionary history.

Right.

This group, despite its incredible diversity, is considered the oldest, well, one of the three major evolutionary lineages within the Ascomycota.

And Ascomycota is one of the biggest divisions of fungi.

Exactly.

Our source material, the Introduction to Fungi, it really describes how DNA sequence data has opened our eyes to their ancient roots.

It's quite something.

That's right.

So our mission for you today is to cut through some of that dense scientific info.

Yeah, make it accessible.

And really understand why these seemingly disparate fungi are grouped together, what makes them unique.

And why they matter.

And why they're so crucial, yeah.

Everything from plant health to, well, fundamental human biology, you're going to walk away with some serious aha moments.

Hopefully.

So to start, just imagine a group of about 150 species.

Okay.

Not huge, number -wise.

Not huge, no.

Across ten genera.

But they look and live so differently, it's actually hard to find common ground just by looking.

That's the challenge, then.

That is the challenge with archaeascomyces.

They include the plant pathogens, taffrina, and protomyces.

Okay.

Plant diseases.

The everyday fission yeast.

Schizosaccharomyces.

Ah, the lab yeast.

That's the one.

Then the human pathogen pneumocystis.

Right.

Serious stuff.

The filamentous neolecta.

It's a bit weird.

Filamentous?

Like mold?

Sort of thread -like, yeah.

And the yeast -like cytowella.

So all over the place.

So what does unite them, then, if not their looks or lifestyles?

Well, okay.

Think about typical fungi.

Many produce these intricate fruiting bodies, right?

Asco -carbs.

Like mushrooms or cup fungi, visible things.

Exactly.

But with archaeascomycetes, with the notable exception of neolecta, they generally lack them.

Mostly no fruiting bodies.

Okay.

Instead, there is scadenas.

Those are the spore -producing sacs.

They're produced individually, often directly from yeast cells or just simple hyphal tips.

Simpler.

Much simpler.

They don't have differentiated ascogynous hyphae, these specialized structures.

And even neolecta, the exception.

Yeah.

What about it?

It's peculiar.

Its fruit bodies lack these sterile filaments called periphyses, you often see.

And it's asco spores.

Get this.

They can bud into yeast -like conedia while still inside the ascus.

Budding inside the spore sac.

Yeah.

It's a strange phenomenon.

And you also see that in tefrina.

Huh.

Okay.

Here's where it gets really interesting for me.

You have these ancient fungi.

Some are simple yeast, single cells.

Others are filamentous, like threads.

Right.

It raises that classic chicken and egg question, doesn't it?

Which form came first, the yeast or the mycelium?

Exactly.

And the fact that you have both yeast -like and mycelial forms in this group, which is considered the most basal, the most ancestral.

Yeah.

It makes it impossible to definitively say which is the ancestral form.

So looking at them doesn't give us the answer.

Not definitively.

It really makes you question how much morphology, just physical form, can tell us about deep evolutionary relationships, you know?

Right.

If the oldest group is already this mixed.

Precisely.

But what is significant, though, is the molecular data, the DNA.

Okay.

Molecular studies consistently place tafrina within this group.

That reinforces its suspected ancestral status.

Which people suspected before DNA?

They did, yeah.

Based on some features.

And Pneumocystis, too.

Its phylogenetic position, where it fits in the tree of life, was debated for ages.

Bouncing between groups.

Yeah, exactly.

Until DNA pretty much settled it here in the archaeoscomycetes.

Okay, let's dive into tafrina, then.

A key player, you said.

Definitely.

You mentioned it's a plant pathogen, so we've probably seen its handiwork.

Oh, almost certainly, even if you didn't know the culprit.

Tafrina species are biotrophic parasites.

Meaning they need a living host?

They need a living host to survive, yeah.

Primarily flowering plants.

And their effects are often quite traumatic.

They cause a wide variety of plant disorders.

Like what?

Think witch's drooms.

Those dense, abnormal tufts of twigs you see sometimes.

Ah, I've seen those on birch trees.

It could be tafrina betulina.

Or galls.

Those strange growths.

And the classic leaf curl diseases.

I have a leaf curl, Frank.

Our source mentions tafrina pruni causing pocket plums.

The fruit shrivels up, has a hollow center instead of a scone.

Weird.

So, how do they pull this off?

What's their life cycle like?

It's pretty cool, actually.

When you isolate them away from a host, tafrina ascospores can just germinate by budding.

They form these saprotrophic haploid yeast cells.

So they can live on dead stuff, too, in that yeast phase.

Yeah, they can manage.

But in the host plant, that's where they form a mycelium.

Intercellular septate hyphae threads growing between the plant cells.

Between, not inside.

And here's a fascinating detail.

The hyphae and tafrina are dicariotic.

Dicariotic.

Two nuclei.

Two nuclei per cell, yeah.

Which is actually quite unusual for ascomycetes.

But typical for?

But very typical of ascidyomyces, the other major group.

Think mushrooms.

It hints at these deep evolutionary connections.

Wow, okay.

The infection sort of culminates with individual hyphal tips undergoing meiosis, making eight haploid ascospores.

And they often get discharged pretty violently from the leaf surface.

Let's take tafrina deformans.

That's the peach leaf curl one, right?

That's the one, very common.

If you've ever had a peach or almond tree, you might have seen this.

You know what I look for.

You'd notice these raised, reddish, kind of puckered blisters on the leaves.

And then they develop this waxy bloom.

A whitish sheen.

Okay, what's the bloom?

That bloom is actually a layer, like a palisade, of the fungus's acaea forming right there on the leaf surface.

The sporesaxe, yeah.

Exactly.

Inside the leaf, meanwhile, the fungus is growing this extensive mycelium between the cells.

And the ascus formation is weird too, you mentioned.

Yeah, it's quite unique.

Two nuclei fuse in a fungal cell.

Okay, then after divisions, you get eight ascus spores.

But they're delimited, sort of walled off, not from the nuclear envelope like usual, but by the invagination, the folding inwards, the developing ascus's own membrane.

It's a different mechanism.

Huh, minor detail, major difference maybe.

It suggests different evolutionary pathways, yeah.

And remember the spores budding inside the ascus.

Tedaformans does that too.

Forms these yeast cells called lullaria.

That's its anamorphic state, its asexual form.

And these tiny fungi can totally warp a plant, right?

How does that even work?

Yeah, it raises an important question.

How does a fungus cause such dramatic distortions?

Seems like magic.

Well, the source explains these distortions are linked to increased cell division and enlargement in the host tissue.

Basically, the plant cells go wild.

But how?

Well, taffrinadeformans is known to produce oxen type phytohormones, plant hormones,

like indole acetic acid inside of cannons, another type of plant hormone when you grow it in culture in the lab.

Oh, plant growth regulators.

Exactly, powerful stuff.

Now, it's not formally proven that the fungus produces these substances in plant, you know, inside the actual living plant.

Right.

But infected leaves do show higher levels of these hormones.

So the suspicion is very strong that the fungus is basically pumping out hormones to manipulate the plant's growth.

Hijacking the system.

Okay, so what does this all mean for gardeners and farmers?

Can you control it?

Absolutely.

Taffrinadeformans is a serious pathogen.

It overwinters as those yeast cells, the lullaria stage, often just on the surface of twigs or in the bud scales.

Waiting for spring.

Exactly.

In spring, as the peach buds open, these yeast cells produce germ tubes, little infection threads that penetrate the young leaves.

See, if I've hit it early.

That's the key.

Control involves spraying with fungicides.

Something like Bordeaux mixture in autumn, after leaf fall, helps reduce that overwintering yeast population.

Minute up, crew.

Kind of.

And then again in early spring as the buds swell.

Because the fungus's infection window is actually quite limited, it generally stops causing new infections by early July.

Okay, so timing is crucial.

Very much so.

Simple fungicides applied then can be quite effective.

Right.

Okay, let's pivot now from plant parasites to something maybe more familiar.

Yeast.

Nice.

But this isn't just any yeast.

This is Schizosaccharomyces, also known as fish and yeast.

Indeed.

And while there are only three recognized species in the genus, S.

japonicus, S.

octosporus, and S.

pombe,

the latter two are especially significant.

S.

pombe is the famous one, right?

That's the one you hear about most.

They're all saprotrophic yeasts.

Meaning they eat dead stuff.

Dead or decaying organic matter, yeah.

You find them in places with lots of soluble carbon sources.

Tree exudates, fruits, honey.

Sweet spots.

Pretty much.

S.

pombe, for instance, is used traditionally to ferment African millet beer called pombe.

That's where the name comes from.

Ah, pombe beer, makes sense.

And aric in Java.

It can tolerate up to 7 % ethanol, so it's pretty robust.

Okay, so how does it get the name fish and yeast?

What's that about?

That's because of its unique way of reproducing asexually, by fiction.

Splitting exactly in half.

Unlike budding yeasts, like baker's yeast, which pinch off a smaller daughter cell.

Right, asymmetric.

Schizosaccharomyces cells divide symmetrically.

Two equal daughter cells.

Neat, and sexually.

For sexual reproduction,

two habloid yeast cells conjugate, they join up, fuse,

undergo meiosis,

and typically produce four or eight ascus spores inside an ascus.

Okay.

And you mentioned something odd about its cell walls.

Yeah, what's fascinating here is that its cell walls are primarily glucans, which is typical enough, but they contain only traces of chitin.

Chitin's the stuff in insect exoskeletons and most fungal walls, right?

Exactly.

So having only traces is quite unusual for fungi.

But that tiny amount of chitin seems to play an important role in making the ascus spore walls.

Huh.

So why is this particular yeast, es pombe, such a big deal in biology?

It seems pretty humble for all the hype it gets.

Yeah, it does seem humble.

But, connecting this to the bigger picture, es pombe is a crucial model organism in biological research.

A lab rat, basically.

Sort of, yeah.

Often compared to its rival, Saccharomyces cerevisiae, the baker's yeast, its whole genome has been sequenced.

Researchers are even trying to figure out the minimum number of genes it needs just to function.

Wow.

And this raises that important question.

Why is a single -celled fungus so critical to understanding complex life, like us?

Tell us, why?

It comes down to the cell cycle.

Es pombe is given as a fundamental understanding of how cells control their division.

How one cell becomes two.

The basics.

The absolute basics.

Imagine a cell going through its phases.

G1, that's growth, no DNA copying yet.

S phase, DNA synthesis happens.

G2, more growth, getting ready.

And M, mitosis, the actual division.

Right, the standard cycle.

Well, es pombe research identify critical checkpoints in this cycle, like the start point in G1, where the cell basically commits to dividing.

And the boundary between G2 and M, deciding when to actually split.

Control points.

Exactly.

And the absolute most fundamental gene involved in this whole process is called CDC2.

CDC2.

Its product is a protein kinase, an enzyme.

And it's involved at both the start point and the G2M control point.

It's like a master switch.

One gene, two key jobs.

And here's the truly astonishing part.

This protein, CDC2 kinase, fulfills the same universal role in all eukaryotes, including us humans.

The same protein.

The equivalent protein, doing the same fundamental job.

Its activity is fine -tuned by other proteins called cyclins, which cycle up and down and by other kinases and phosphatases that respond to signals from the environment or inside the cell.

So studying this tiny fish in yeast has revealed mechanisms that are literally keeping us alive.

Right.

And preventing diseases like cancer.

That's mind blowing.

Precisely.

The principles uncovered in es pombe are conserved.

They apply across the board.

For example, in mammals, if your DNA gets damaged, that can stop the cell cycle at that G2M checkpoint.

Get the breaks.

Exactly.

And it can trigger apoptosis program cell death,

which is a crucial protection against uncontrolled cell growth.

Which is cancer.

The very basis of cancer.

This groundbreaking work on es pombe, figuring out these controls.

It even led to Sir Paul Nurse getting the Nobel Prize in Medicine and Physiology back in 2001.

Wow.

From a yeast on African beer to a Nobel Prize.

Incredible, isn't it?

And it's not just the cell cycle, right?

This yeast is also teaching us about how cells grow and maintain their shape.

Yes, absolutely.

It's morphogenesis, how it builds itself, provides insights that are relevant even to filamentous fungi.

Es pombe cells are rod shaped.

They initially grow just at one end.

Okay.

Then later they switch to bipolar growth, growing from both ends.

And this is all coordinated by structures inside the cell, particularly microtubules.

The cell's internal skeleton.

Kind of like tiny internal scaffolds, yeah.

They guide this polarized growth.

They even transport key proteins to the right places.

Then when the cell gets ready to divide, its internal skeleton completely remodels.

Microtubules form this intranuclear spindle to separate the copied nuclei accurately.

And actin, another protein.

Muscle protein, basically.

Similar protein, yeah.

It forms a ring right in the middle that helps the new cell wall of the septum grow inwards, precisely dividing the cell.

Wow.

It's like a little construction project.

It really is.

So this tiny yeast offers a blueprint for how many eukaryotic cells organize themselves, grow, and divide.

Really fundamental stuff.

Amazing.

Okay, our final deep dive takes us into a truly unusual fungus.

Pneumocystis.

Ah, yes.

A very different beast.

If you're involved in healthcare or maybe know someone who is immunocompromised, this one is particularly relevant.

Absolutely.

Pneumocystis lives as these cyst -like cells, but it lives in the lungs of mammals.

In our lungs.

Or other mammals, yeah.

And it's notoriously difficult to study because you can't really grow it in a lab dish outside its host.

Ah, makes research tough.

Very tough.

Its identity as a fungus was only confirmed relatively recently through DNA sequencing.

For years, people weren't sure what it was.

Really?

Yeah.

Different species are found in different hosts.

For humans, the pathogen is Pneumocystis jirovici, named after the scientist Jirovac.

And it causes a severe form of pneumonia, often called PCP, especially in immunocompromised individuals.

It's actually considered an AIDS -defining illness because it was so common and severe in untreated HIV AIDS patients.

Serious threat.

Definitely.

And what's fascinating here is the uncertainty around its epidemiology, how it spreads.

There's no convincing evidence of an external reservoir, like in soil or water.

So it doesn't live outside a host.

It seems to spread primarily, maybe even exclusively, human to human, probably through the air.

Wow.

Okay, so what makes this fungus so odd, then, beyond its habitat inside us?

Well, it has several peculiarities.

Adaptations, really.

First, unlike most fungi, Pneumocystis lacks ergosterol.

Ergosterol.

That's the main sterol in fungal membranes, right?

Like, cholesterol is for us.

Exactly.

Fungi use ergosterol.

Pneumocystis uses cholesterol instead, which it probably gets from the host.

So it uses our sterol.

Seems like it.

And this explains why it's insensitive to Infotericin B.

That's a really important antifungal drug.

Yeah, heard of it.

But it works by targeting ergosterol.

So no ergosterol, no effect.

Makes sense.

But some drugs do work.

Yes.

It is susceptible to drugs that inhibit beta, 1 -benin -3 -glucan synthesis.

Glucans are key parts of its cell wall, which is unusually thin, by the way.

Okay, so attack the wall.

Attack the wall synthesis, yeah.

Secondly, and this is quite remarkable, it only has two ribosomal RNA gene repeat units.

Two.

How many do other fungi have?

Usually 50 to 250 copies.

Whoa, that's a huge difference.

Why so few?

It's a great question.

It raises important questions about its minimal genetic requirements.

It suggests extreme genetic streamlining, maybe because it's so highly adapted to its barotenic lifestyle inside the lung.

It might rely on the host for a lot.

Fascinatingly weird.

Okay, so let's pull this all together.

What does this entire deep dive into archaeascomycetes mean for you listening?

Well, we've explored the archaeascomycetes, right?

A group of fungi that are truly ancestral, deep on the fungal tree of life, and incredibly diverse.

Yeah, really diverse.

From taferina causing these dramatic diseases in plants, maybe by producing plant hormones.

Leaf curls and witch's brooms.

This gets to Saccharomyces pombe, the fish and yeast,

unlocking these universal secrets of the cell cycle.

Secrets that literally earned a Nobel Prize.

Amazing impact from a simple yeast.

And finally to Pneumocystis, this strange lung -dwelling fungus with really unique biology that poses a serious threat to human health, especially for vulnerable people.

So this deep dive really shows us that even these seemingly obscure organisms, things most people have never heard of.

They can hold fundamental keys to understanding life itself.

They influence our ecosystems, our agriculture.

And even our own cellular processes, as we saw with the cell cycle.

They really challenge our neat biological categories sometimes too.

Yeah, absolutely do.

And if we connect this to the bigger picture, it just underscores that the world of fungi is far more complex and far more impactful than just mushrooms on a log.

Right, there's so much more going on.

These oddball Archaeoschema cices, they really demonstrate the profound insights that can come from studying life at its most fundamental levels.

It shows how closely intertwined fungal biology is with our own health and the health of the whole planet.

We hope this deep dive into Archaeoschema cices has given you some surprising facts.

Maybe a few aha moments, like we promised.

And perhaps a shortcut to being well informed about this really fascinating ancient corner of the fungal kingdom.

It's a glimpse into the deep history of life.

It really is.

Thank you for joining us on the deep dive.