Chapter 2: Protozoan Pseudofungi, Chromistan Pseudofungi, and Early True Fungi

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Welcome, curious minds, to another deep dive.

Ever thought you knew what a fungus was?

We might be surprised by how many organisms look like fungi, but are actually quite different.

Today we're taking a really fascinating journey into a mixed bag.

That's chapter two from Brace Kendrick's incredible book, The Fifth Kingdom.

Our mission for you is to distill the key insights here, help you confidently tell true fungi from their imposters,

and understand why these differences matter.

And we're going to do it all without needing a single diagram.

Okay, let's unpack this.

Yeah, and it's a journey that really highlights, well, the detective work of science, doesn't it?

For centuries, even trained scientists were fooled by just looking at them, superficial similarities.

Imagine trying to figure this out with limited tools.

It's easy to see why they were all kind of lumped together initially.

But as our understanding grew, looking deeper beyond just what you see became absolutely crucial for getting the classification right and understanding their true place in the big picture.

That point about looking deeper is so important.

So when we did finally look beneath the surface, what were the fundamental sort of must -haves that define a true fungus?

What sets them apart from all these mimics?

Okay, so at their core,

true fungi are heterotrophic eukaryotes.

Okay, heterotrophic eukaryotes.

What does that mean in simple terms?

Right, so unlike plants, they don't make their own food, they get nutrients from outside sources.

And eukaryotes means their cells have a proper nucleus, other complex bits inside.

Gotcha.

And they don't eat like we do.

No, not really.

They absorb their food directly from whatever they're growing on or in.

We call that osmotrophy.

Think of them like tiny, incredibly efficient sponges soaking up nutrients.

Oh, osmotrophy, okay.

And this absorption often happens through lots of growing points on their body, which is usually diffuse.

We call this body a thallus, or more commonly, a mycelium.

And that's made of?

Tiny branching tubes called hyphae.

That's the classic fungal structure for many of them.

Right, hyphae.

And their cell walls.

Cell walls give them protection.

They're generally made of chitin in the main group, the umicota, or sometimes cellulose like in the umicota, which we'll definitely get to.

Chitin, okay, like insects have.

Exactly.

And critically, they reproduce using spores, tiny reproductive units.

Okay, that paints a clear picture of the real deal.

But before we dive deeper into those fungi,

we absolutely have to talk about the outsiders, right?

The ones mistakenly put in the fungal box.

We do.

And what's fascinating here is how these groups, even if they look similar on the surface, are fundamentally different inside their cells, their life cycles, completely different paths.

The source material calls them the so -called slime molds.

And you'll definitely see why that name fits their often quite gooey nature.

So this mixed bag,

where do we even start sorting?

Which groups were the big foolers initially?

And what did we learn about them?

Well, the very first ones that caused confusion were actually more like, well, shapeless blobs.

They belong in kingdom protozoa, totally different from true fungi.

The key distinction for these protozoan pseudofungi is that their main feeding stage is amoeboid.

Just think of tiny oozing shapes moving around.

Amoeboid.

Like an amoeba.

Exactly.

And crucially, they don't have true hyphae, those branching tubes we just talked about, and their amoeboid bodies.

No cell walls during that feeding phase.

That's a massive difference right there.

Okay, no hyphae, no cell walls in the feeding stage.

So let's start with the phylum mixostelida.

The source calls them the real slime molds.

These sound pretty wild.

Oh, they are.

If you're out looking for fungi in autumn, you might actually stumble upon these.

Their feeding phase is this macroscopic, you can see it slimy, amoeboid mass.

It's called a plasmodium.

A plasmodium.

Like the malaria parasite.

Same name, totally different organism.

This plasmodium is full of diploid nuclei, just oozing, shimmering almost across soil or decaying wood.

And it engulfs its food bacteria, tiny particles.

It doesn't absorb, it eats.

Wow, okay.

Engulfing, not absorbing.

Right.

You could even keep some in a pastry dish.

Feed them rolled oats.

It's quite something to watch.

You can keep them as pets.

That's amazing.

Yeah.

And then this plasmodium undergoes this really dramatic transformation.

It morphs into stocked, dry structures called sporangia, packed with powdery resting spores.

So it goes from wet slime to dry stocks.

Exactly.

And the life cycle is intricate.

Tiny haploid spores can germinate into cells that act as gametes.

They fuse, form a diploid zygote, and that grows back into that amazing plasmodium.

It's a whole shape -shifting cycle.

It has a wild transformation.

Okay.

Next up, phylum Dictyostelida, the cellular slime molds.

Dictyostelium discoidium is the famous one here, isn't it?

It absolutely is.

And it's a real marvel of biology.

In its feeding phase, Dictyostelium exists as just individual, independent amoebae, each one munching on bacteria doing its own thing.

Okay, separate amoebae.

But here's where it gets really cool.

When food runs low, they start secreting a chemical signal.

It's CamMP, cyclic adenosine monophosphate.

CamMP, like the signaling molecule in our cells.

The very same.

It acts like an SOS signal here.

Thousands of these individual amoebae sense it and stream together, forming these aggregations called pseudoplasmodia, or slugs.

Slugs.

Okay, but pseudoplasmodia, how's that different from the Mixostelida plasmodium?

Crucial difference.

In these slugs, each amoeba keeps its own cell membrane.

They clump together, but they don't fuse into one giant cell like the true plasmodium.

Ah, so it's a multicellular aggregate, not one big cell.

Exactly.

These slugs then crawl around as a unit, find a good spot, usually somewhere drier, and then differentiate into a structure called a serocarp.

It has a thin cellulosic stalk holding up a ball of spores.

Wow, so they go from individuals to a cooperative slug to a reproductive structure.

Precisely.

It's an amazing example of how single cells can organize and differentiate, which is why it's a favorite for scientists studying development.

Fascinating.

Okay, moving on.

Phylum labrinathilida causes eelgrass wasting disease.

Yeah, these are quite different again.

They are spindle -shaped cells, no cell walls, naked cells, basically.

And they live and glide around inside this network of narrow, tubular sheaths made of polysaccharide that they secrete themselves.

Living in their own secreted slime tubes.

Sort of, yeah.

Their main claim to fame, unfortunately, is causing a wasting disease in eelgrass, Zostera.

That's one of the few flowering plants that lives fully submerged in the ocean.

Okay.

And the last of these, Trotazoan pseudofungae.

Phylum plasmodia forida, known for clubroot.

Sounds ominous.

It is for cabbage farmers.

All members of this group are obligate parasites.

They have to infect a host to survive.

Obligate parasites, got it.

The classic example is Plasmodia forabrasicae.

It causes the serious clubroot disease in cabbage and related plants.

How does it work?

Well, tiny zoospores with one flagellum penetrate a root hair of the cabbage.

They grow inside, then release new zoospores.

These ones with two flagellas, okay?

These can swim off and reinfect other roots.

Eventually, inside the root cells, they form these multinucleate structures that break up into incredibly tough cysts.

These cysts get released into the soil and can survive for many years waiting for another cabbage plant.

And the clubroot name.

Ah, right.

The parasite actually stimulates the cabbage root cells to divide and enlarge uncontrollably.

So the roots become grossly swollen, deformed, kind of club shaped.

Hence, clubroot really damages the plant.

Okay.

So we've met these incredible amoeboid organisms.

They definitely fooled early scientists, but clearly not fungi,

mainly because they're amoeboid, lack true hyphae, lack cell walls when feeding.

Now you said things get even more confusing.

We're moving to a group that looks even more like fungi.

Exactly.

Hold onto your hats because now we enter the realm of the chromastan pseudofungi.

These look and in some ways act very much like true fungi, but genetically they're way off.

They're actually related to things like brown algae.

Brown algae.

Like seaweed.

No way.

Yes way.

They're classified in kingdom chromista.

It's a fantastic example of convergent evolution life finding similar solutions,

like growing in threads in completely different branches of the evolutionary tree.

Okay.

Mind blown already.

Let's dive into the first chromastan group.

Phylum hyphocatrio mycota.

Sounds complicated, but you said they have fungal like traits.

They do superficially, at least.

They share quite a bit with a group of true fungi called chytridium mycota, which we'll meet later.

Sup, Jess.

Well, they often live in fresh water or soil.

They can be parasites or sap robes living on dead stuff.

Their bodies can be simple, converting entirely into a reproductive structure, holocarpic, or they can have root -like rhizoids anchoring a sporangium, eucarpic, and they release swimming zoospores with a single flagellum.

Sounds pretty fungal, right?

Yeah, that sounds very much like the description of true fungi earlier.

So what's the

flagellum?

It's the crucial difference, and you can even see part of it with a good light microscope.

In the hyphocatrio mycota, that uniflagellate zoospore has its flagellum attached at the front of the cell.

At the front.

Yes, pulling it along, kind of like a swimmer's arm doing the crawl stroke, and if you look closer with an electron microscope, you see it's a tinsel flagellum.

It has these fine, hair -like filaments along its sides called mastogonyms or flimmers.

Okay, front -facing tinsel flagellum.

How does that compare to the true fungi, the catridiomycetes?

Completely different.

True catridiomycetes also have a single flagellum on their zoospores, but it's always at the back, the posterior end, and it's a whiplash flagellum.

It's smooth, no hairs, and it pushes the cell from behind, like a tail.

So the position and the structure of that single flagellum are the dead giveaways.

Precisely.

These might seem like tiny details, but flagellus structure and arrangement are considered extremely conservative evolutionary traits by biologists.

Meaning they don't change much over time.

Exactly.

They're thought to remain stable over vast stretches maybe hundreds of millions of years, so they're incredibly important clues for figuring out evolutionary relationships.

It tells us these hyphochytriomycotas are on a totally different evolutionary path from true fungi.

Oh, okay.

Any common examples?

Sure.

Hyphochytrium catenoids is pretty common in soil.

Interestingly,

it might actually help control some other fungus -like organisms, the umicota, which can cause plant diseases.

Okay, so we've seen some convincing fakers, these chromosomes, but I get a feeling this next group, the umicota, is where things really escalate in terms of, well, real world impact.

Why are they so notorious?

Ah, the umicota, yes, they definitely earn their notoriety.

You might know them as water molds or downy mildews.

They have several key features that absolutely separate them from true fungi, the umicota.

Okay, lay them out for us.

What are the big differences?

First, there's zoospores.

They typically have two flagella, not one or none, and these two flagellas arise from the side of the zoospore.

Two flagella from the side.

That's unusual.

Very, and they're different types.

One is a tinsel flagellum, like we saw in the hyphochytrids, usually pointing forward.

The other is a whiplash flagellum, smooth, usually pointing backward.

This combination is unique to them.

Okay, unique flagella setup.

What else?

Second, their nuclei.

Unlike all true fungi, the main growing threads, the hyphae of umicetes, contain diploid nuclei.

They have two sets of chromosomes throughout their main life stage.

True fungi are typically haploid or dekaryotic in that stage.

Diploid nuclei in hyphae.

Got it.

And cell walls.

Third, cell walls.

Primarily made of a cellulose -like material, sometimes with a bit of chitin, but mostly cellulose.

Again, a contrast to the largely chicken walls of true fungi.

Cellulose, like plants.

Interesting.

And the name umicota.

Ah, yes.

That comes from their sexual reproduction, which is feature number four.

It's oogomus.

This means they form distinct male structures, antheridia, and female structures, oogonia, containing eggs.

Fertilization leads to a thick -walled resting spore called an oospore.

That oospore is really important for their survival.

Okay, so different flagella,

diploid hyphae, cellulose walls, and oogomus reproduction with oospores.

A very distinct package.

And you said, very impactful.

Hugely impactful.

If we connect this to the bigger picture, you'll see why these aren't just, you know, boring academic details.

They have profound ecological and especially economic consequences.

These organisms, even though they're microscopic individually, can form vast networks of hyphae.

You might see them as that whitish fur coat on a dead fish in a pond, or, much more devastatingly, wiping out entire crops.

You're not kidding about devastation.

Let's get into some specific examples.

Starting with the order sapolinialis, the water molds.

What do they do?

The classic example here is saprolenia parasitica.

It's infamous for attacking fish, especially injured ones, and also fish eggs and hatcheries.

That fuzzy white growth on a dead fish, often saprolenia.

Okay, fish attacker.

How does it reproduce and spread?

Asexualy, it produces these structures called mitosporangia.

These release the biflagellate zoospores we talked about, sometimes called swarm spores.

They actively swim around using those two flagella.

Looking for a fish.

Exactly, or some other food source.

They swim for a bit, and then they can insist stock swimming, pull in their flagella, and form a protective wall.

And then what?

Well, here's a neat trick.

Later, they can often regerminate from that cyst, forming a secondary zoospore that swims off again.

It's like having a second chance to find food if the first swim didn't work out.

A second chance strategy.

Very clever.

And sexually.

Sexually, they undergo that oogmus reproduction we mentioned, forming those tough ooglospores.

These are really resistant and can survive harsh conditions, like if the pond dries up over summer or freezes in winter, ready to germinate when conditions improve.

Very effective survival strategy.

Okay, now for the order of pyranosporalis.

You called these the true crop devastators.

Sounds serious.

They absolutely are.

Many members here are obligate parasites of higher plants, and they are responsible for some of the most catastrophic plant disease epidemics in history.

Why are they so devastating?

Well, partly because of us.

Our modern agricultural practice of growing vast areas of just one crop species.

Monoculture creates a huge uniform target for them.

Plus, many spread very effectively through the air via their mitosporangia, which are sometimes mistakenly called knidia.

Wind can carry them for miles.

Okay, monoculture makes it worse.

Let's talk specifics.

Damping off disease caused by pythium.

I've heard that it kills seedlings, right?

That's the one.

A very common headache for gardeners and greenhouse growers.

Pythium species live in most soils, just decomposing dead stuff.

But when conditions are wet, they produce zoospores that swim through the soil water.

And find young plants.

Exactly.

If they find a young, tender seedling, they infect it, often right at the soil line.

They release toxins and, crucially, an enzyme called pectinase.

Pectinase.

What does that do?

Pectin is like the glue that holds plant cells together in the middle lamella.

Pectinase dissolves it, so the plant tissues basically fall apart, rot very quickly, and the seedling collapses at the base.

That's damping off.

Nasty stuff.

How do people control it?

Often by using heat -sterilized soil, especially for seedlings, or by applying specific fungicides.

Good drainage also helps, as the zoospores need water to swim.

Right.

Avoid soggy conditions.

Okay.

It's truly sobering how much damage these can cause.

And speaking of damage,

the next one.

Late blight of potato caused by Phytophthora infestans.

This one is infamous, isn't it?

It changed history.

It absolutely did.

This umisi, originally from North or Central America, caused the devastating Irish potato famine in 1845 to 1847.

The Great Famine.

Yes.

Potatoes were the staple food for much of the Irish population.

When this disease hit, it completely wiped out the crop year after year.

It led to the deaths of about a million people from starvation and disease, and forced another million or more to emigrate.

Changing Irish history and demographics forever.

Unbelievable.

Just from one microscopic organism.

It's staggering.

And that event really kickstarted the whole field of plant pathology.

The scientific study of plant diseases, people realized they needed to understand these things.

But it's not just history, right?

You mentioned it's made a comeback.

Alarmingly, yes.

For a long time after the famine, Phytophthora infestans in Europe and North America was mainly reproducing asexually.

It needed two different mating types for sexual reproduction via oospores, and only one time was widespread outside its native Mexico.

But then probably around 1976, the other mating type was accidentally imported, likely on infected potatoes.

Suddenly, the pathogen could reproduce sexually again, forming those resistant oospores and, crucially, generating new genetic combinations.

Leading to new, maybe more aggressive strains.

Exactly.

We've seen new, highly aggressive strains emerge, resistant to some older fungicides.

It's now a constant battle.

It cost the US alone something like $3 billion a year, just in control efforts and crop losses for potatoes and tomatoes.

$3 billion a year, wow.

And Phytophthora is a nasty genus overall.

P.

sodos hit soybeans.

P.

megacaria devastates cacao in Africa.

There's a hybrid killing alder trees across Europe.

P.

cinnamomi is destroying native forests in Australia and parts of Spain, plus causing root rot in avocados, pineapples.

The list goes on.

It's a global menace.

What a profound, ongoing impact.

Okay, another historical one.

Downy mildew of grape.

Plasmaparavidicola.

What's the story there?

Another fascinating case of introduced disease.

Plasmaparavidicola is native to North America, where it lived in relative balance with native wild grapes, which had evolved some resistance.

Okay, coevolution.

Right.

But then, sometime in the 1870s, it was accidentally introduced to Europe, probably on imported American vines.

The European wine grape, Vitis vinifera, had absolutely no resistance.

Oh dear.

For the French wine industry.

It was catastrophic.

The disease spread like wildfire, threatening to wipe out the French vineyards, the heart of their wine industry.

Panic ensued.

But there was a solution.

Fortunately, yes.

A professor at the University of Bordeaux, Pierre Millardet, noticed that vines near the roadside, which had been sprayed with a mixture of copper sulfate and lime to deter grape thieves, weren't getting the mildew.

He experimented and perfected the recipe, creating what became known as Bordeaux mixture.

It was basically one of the world's first effective practical fungicides.

It saved the European wine industry.

A true hero moment in plant pathology.

A toast to Bordeaux mixture, then.

Okay, quickly.

Blue mold is tobacco.

Paranosperatavecina.

This one caused major epidemics, for instance, in Ontario, Canada, in 1979.

Wiped out about $100 million worth of tobacco.

Often these outbreaks were triggered by importing infected seedlings from warmer regions, combined with cool, wet weather favoring the pathogen.

It was definitely a factor in the decline of the tobacco industry in some areas.

And lastly, for the Paranosperalis.

White rust disease, El Bugo Candido.

This one attacks cruciferous plants in the cabbage family, like cabbage itself, radish, mustard, shepherd's purse.

You see these characteristic white blister -like pustules on the leaves and stems.

Like a rust, but white.

Exactly.

Those blisters are packed with chains of mitosporangia.

They break open, the sporangia get dispersed by wind or rain splash, and each one can germinate in water to release about eight of those biflagellate zoospores we keep mentioning, ready to start new infections.

Wow, those chromista, especially the Umicota, they really are major players.

They've shaped agriculture, economies, human history.

But now finally, let's talk about the organisms that truly belong in the fungal kingdom.

The Umicota.

The real deal.

Yes, finally.

The true fungi.

So what defines kingdom Umicota, setting them apart from all those pseudo -fungi and chromistans?

Genetically, they are a distinct group.

Universally, they possess chitin in their cell walls.

That's a big one.

Chitin walls, okay.

And they also share the same biochemical pathway for making the amino acid lysine.

It sounds technical, but it's another fundamental marker of their shared ancestry, different from plants and chromistans.

Chitin walls and a specific lysine pathway.

Got it.

Now, some of these true fungi also have flagella, right, like the et ceteras you mentioned earlier.

They do.

Several of the phyla, considered to be early diverging branches of the Umicota, have flagellate stages, usually zoospores or gametes.

So understanding flagella is still important here.

And you mentioned something incredible about flagella structure before.

Yes, it bears repeating because it's so fundamental.

Flagella are these long, whip -like structures that let cells swim, often towards food or a mate following chemical trails.

But the truly amazing thing, the mind -blowing thing, is that across almost all eukaryotes, fungi, animals, protists, even some algae wherever you find this type of flagellum, it has an essentially identical internal structure.

This intricate 9 plus 2 microtubule pattern.

Nine pairs around the outside, two in the middle.

Exactly.

Nine pairs of microtubules forming a cylinder around two central single microtubules.

It's incredibly complex and incredibly tiny, about one sixth of a micron thick.

You could line up a hundred thousand of them side by side and they'd be less than an inch wide.

Wow, and the same structure is in.

Human sperm tails, the cilia lining our windpipes, the flagella of paramecium, green algae.

It's a profound signature of our shared eukaryotic ancestry.

It tells us we're all related.

Deep gown.

Bacterial flagella, by the way, are totally different structures, built differently, evolved independently, but that's another story.

Truly mind blowing to think about that shared microscopic engine across such a diverse life.

Okay, so within the true fungi,

the eumicota, let's start with phylum 1, chytridiomycota.

What's their defining flagellar feature?

Right, the chytridiomycota, or chytrids.

Their key feature is that their asexual zoospores have a single backwardly directed whiplash flagellum.

Single posterior whiplash, got it, like a tiny tadpole.

Exactly, always pushing from behind, smooth flagellum.

Now their body forms, their somatic phases, can vary quite a bit.

How so?

Some are very simple, holocarpic, the entire cell basically just swells up and becomes a reproductive structure, asperangium, releasing zoospores.

Olpidium brassicae, which lives in cabic roots, is like this.

The whole thing becomes reproductive, okay.

Others are eucarpic.

This means our body differentiates into distinct parts.

An assimilative part usually find root -like threads called rhizoids, which anchor it and absorb nutrients but don't contain nuclei.

And one or more reproductive parts, the sporangia.

Chytridium and spizel mysis are examples.

Rhizoids for feeding, sporangium for reproducing, makes sense.

And you mentioned rhizomycelium.

Yes, some chytrids develop a more extensive network of threads than just simple rhizoids.

This is called a rhizomycelium.

It's different from true mycelium made of hyphae, but it's more branched than rhizoids, and importantly, it does contain nuclei.

It can spread through the substrate and nourish multiple sporangia.

We call that polycentric.

Cladocatrium is an example.

Okay, so rhizoids are simple, no nuclei.

Rhizomycelium is more complex, has nuclei, supports multiple sporangia.

Gotcha.

What sort of things do these chytrids do?

They're everywhere, doing all sorts of things.

Some, like spizella mysis and chytridium, are often found parasitizing pollen grains that fall into water.

Cladocatrium is cyprobic, decomposing dead plant matter in aquatic environments.

Any important pathogen?

Yes,

definitely.

Zynchytrium endobioticum causes wart disease of potato.

It infects the tubers, causing these ugly dark brown cauliflower -like growths that make the potatoes unusable and reduce yield significantly.

It's a reportable disease in many countries.

Potato wart, okay.

And this brings us back to that question you raised.

Why are these tiny organisms sometimes causing such big problems now?

Because I know the big devastating example involves chytrids and frogs.

Exactly, the frog problem.

It's a major global conservation crisis.

A specific eucarpic hydride, Betracholcatrium dendrobotitis, often congreed for short, is causing a devastating disease in amphibians worldwide called chytridiomycosis.

How does it harm the frogs?

It infects the keratinized cells in their skin.

Frogs, as you know, absorb water and electrolytes and even breathe partially through their skin.

The fungus causes the skin to thicken abnormally, interfering with these vital functions, often leading to death.

That's terrible, but why now?

Hasn't this fungus always been around?

That's the million dollar question, and the answer is still debated.

One hypothesis is that the fungus itself has been spread around the world relatively recently, maybe by human activities, trade in amphibians, even researchers carrying spores on their boots.

Okay, novel pathogen hypothesis.

Another idea is that the fungus might have been around, but frogs' immune systems are now compromised, making them more susceptible.

Why?

Maybe environmental changes like increased UV radiation from ozone depletion, pollution from pesticides or other chemicals, climate change.

It could be a combination of factors.

It's a really stark reminder of how fragile ecosystems can be.

Truly sobering.

Do chytrids reproduce sexually, too?

Some do.

A classic example studied is monobluphorus polymorpha.

It shows ugami, similar in principle to the umi seeds, but evolved independently.

It produces motile male gametes, basically sperm, which fertilize a non -motile female gamete, an egg or oosphere.

Okay, ugami.

Any interesting twist?

Well, in monobluphorus, the male gametes are often released before the female egg is fully mature and receptive.

This timing difference seems to be a mechanism to promote outbreeding or heterothalism fertilization between different individuals, rather than cell fertilization.

Increases genetic diversity.

Clever strategy.

So evolutionarily, where do the chytrids fit?

They're considered to represent a modern survival of the kind of ancestral fungi that likely gave rise to the other major groups of Umicota, the ones that lost flagella.

They retain that primitive, flagellate character.

So they're like a window into the past of fungal evolution.

In a way, yes.

Although things are always being updated, recent molecular studies have shown that some organisms traditionally placed with chytrids like alpidium and rosella are actually quite distinct.

Rosella, in fact, might represent the earliest diverging lineage of all fungi, perhaps even deserving its own phylum, maybe called Cryptomycota.

Science marches on.

Wow.

Constantly redrawing the map.

OK.

Moving on to phylum two.

Blastopladiomycota.

This was once grouped within the chytridiomycota, you said.

That's right.

For a long time, they were considered in order within the chytrids.

But molecular data, especially DNA sequences, showed they were distinct enough to warrant their own phylum, established formally around 2006.

What makes them different?

Their thallus, their body, is a bit more complex.

It typically has both broad, true hyphae alongside narrower rhizoids.

A really well -studied example is Allomyces arbusculus.

What's special about Allomyces?

It has this really clear alternation of generations, a life cycle that rotates between distinct haploid and diploid thalli, or bodies.

Like plants do.

Similar concept, yeah.

The haploid thalli produce gametes in specialized structures called gametangia.

And Allomyces shows anisogamy.

Anisogamy, meaning unequal gametes.

Exactly.

The gametes come in two different sizes.

There's a smaller, more mobile male gamete that actively seeks out a larger, less mobile female gamete.

The female gamete contains more food reserves for the resulting zygote.

It's seen as a step towards distinct sperm, and egg is a division of labor.

OK.

Anisogamy on the haploid stage.

What about the diploid stage?

The diploid thalli, which grow from the zygote, produce two kinds of sporangia.

Thin -walled mitis sporangia release diploid zoospores that just grow into more diploid thalli.

That's asexual reproduction.

But they also produce thick -walled brownish, very resistant myosporangia.

Resistant ones.

Yeah.

For survival.

Yes.

These can survive harsh conditions, sometimes for decades.

When conditions are right, meiosis happens inside them, and they release haploid myospores, which then grow into the haploid gamete -producing thalli, starting the cycle again.

Fascinating alternation.

Any practical relevance for this group?

Well, another member of this phylum is the genus Colomomyces.

These are obligate parasites, but interestingly, they target mosquito larvae.

So there's active research into potentially using them as a form of biological control against mosquitoes.

Using a fungus to fight mosquitoes.

Cool.

OK.

And finally, phylum three.

Neocalmistigami coda.

This sounds like the newest addition.

It is indeed.

These were a complete surprise, only discovered in 1975.

And where were they found?

In the rumens, the digestive tracts of large, herbivorous mammals like cows and sheep.

Living inside cows.

Yeah.

They have some really unique features.

First, they are obligately anaerobic.

They cannot survive in the presence of oxygen.

The rumen is an oxygen -free environment.

OK.

Strict anaerobes.

Second, they have no mitochondria.

That's highly unusual for eukaryotes.

Mitochondria are usually the powerhouses of the cell using oxygen.

These fungi have different organelles, hydrogenosomes linked to their anaerobic metabolism.

No mitochondria.

Wow.

Anything else?

Many of them have multiflagellate zoospores.

Instead of just one flagellum, like the chytrids, their zoospores can have many.

And what are they doing in the rumen?

They play a crucial role in digestion for the host animal.

They produce rhizomycelia that physically penetrate tough plant material the animal has eaten.

And they produce incredibly powerful enzymes that break down cellulose and other plant fibers, arguably more effectively than any other known microbes.

They are essential partners for these herbivores.

Amazing symbiosis.

OK.

So as we wrap up this pretty intense journey through a mixed bag today,

what does this all mean for you, our listener, as a learner?

Well, this deep dive has definitely shown us the incredible, almost bewildering diversity hiding under the simple word fungi.

We went from those truly amoeboid pseudo fungi, the slime molds, to the chromosome imposters like the umicota, which mimic fungi so well with their hyphae and spores, but are actually related to algae.

Right.

All the way to the flagellate members of the true fungal kingdom, the umicota, like the chytrids and their relatives.

And I think the key takeaway is really clear.

Not everything that looks like a fungus is one.

You really have to look closer.

Absolutely.

The critical differences aren't superficial.

They lie in fundamental cellular things, the structure of flagella, what the cell walls are made of, whether the nuclei are haploid or diploid during the main growth phase.

And we've seen just how powerful these organisms are, haven't we?

Shaping history through famines, devastating crops, causing ecological crises like the current frog problem.

It's not just taxonomy.

It has real world weight.

It really does.

And this deep dive, I think, shows us how science works, how our understanding of life is constantly being refined, especially with new tools like molecular analysis.

The ability to look at things that seem similar on the surface and find those profound defining differences underneath.

That's really the heart of scientific discovery, isn't it?

Beautifully put.

And maybe a final thought to leave you with.

Considering how much discovering these outsiders, the pseudo fungi, the chromastans, has reshaped history or forced us to rethink taxonomy, what other biological classifications, maybe ones we take for granted now, might be due for a radical rethink as new scientific evidence comes to light, and what unexpected real world consequences might those future shifts reveal.

Ooh, that is a provocative thought to chew on.

What else are we getting wrong right now?

Well, thank you for joining us on this deep dive into this fascinating mixed bag of microscopic wunchers.

We really hope you've gained some valuable insights and maybe a newfound appreciation for the sheer incredible diversity of life out there.

From all of us here at the deep dive and your last minute lecture team, happy exploring.