Showing posts with label amphibian. Show all posts
Showing posts with label amphibian. Show all posts

Wednesday, January 7, 2015

The Fungus And The Frog

Biology concepts – common descent, evolution, direct descent, fungi, undulipodia, amphibians, phylogenetics

THIS IS NOT HOW EVOLUTION OCCURS!! What this
animation implies is that one type of animal became
another type of animal. It shows a chimp becoming a
human. If so, how come there are still chimps? This
suggests direct descent with adaptation and this is a
fallacy. What is correct is that the animals shown did all
share a common ancestor at some point.

The first life on Earth is a mystery to us. Our best guess right now states that whatever it was, it showed up about 3.5-3.7 billion years ago. It was a cell, let’s call him Luca (last universal common ancestor). Luca had DNA, or maybe just RNA. He had ways to harness and use energy for his purposes, to adapt to changes in his environment, and to reproduce. Luca possessed all seven of the characteristics of life.  

Every living thing you see around you, and all the living things you can’t see around you, are descended from Luca. But here is the part that’s a little harder to understand – it hasn’t been a straight line from Luca through all other life forms to you.

It’s the difference between common descent and direct descent. Just because humans and pine trees have a common ancestor, it doesn’t mean that we are direct descendents of the same organism.

At some point, about 3.5 billion years ago, archaeal prokaryotes were recognizable. Luca gave rise to archaea and also to bacteria, but we can’t say that bacteria descended directly from archaea. There are as many differences between archaea and bacteria as there are between you and a pine tree, maybe more. All we can say is that they diverged from a common ancestor, which is why they have some common characteristics (from a common ancestor), and many different characteristics (because they diverged).


This is a much better representation of evolution
through common descent and adaptation. We may not
know what exact organism was the last common ancestor
between any two branches since only the fossil record only
represents about 1% of species that lived.
Bacteria were, and are, just about perfect organisms. They were bacteria then, and they are bacteria now - why mess with perfection. They have diverged into many types of bacteria, and those types are diverging even today, but they have stayed as bacteria.

Archaea, as opposed to bacteria, diverged again and again, giving rise to the rest of the kingdoms we know today – protists, plants, fungi, and animals. The question is, why did they diverge so much, while bacteria stayed so much the same?

I don’t know the answer, but a good theory is the development of organelles. We have talked before about how an archaea swallowed a bacteria, but didn’t destroy it, and how that the eukaroytic nucleus. Another instance in this endosymbiosis theory formed the mitochondrion. The more complex something is, the more chance for it to respond to changes in the environment – more adaptation could have led to more divergence.

Through billions of years of struggle and adaptation, the eukaryotic kingdoms emerged – but again, you can’t say that one descended directly from another. Contrast evolution to the alphabet. C follows B, which follows A. Humans like to think linearly. But consider that there may be millions of A’s. Must they all become B’s and then C’s?

No, millions of A’s may breed and remain A’s over the years, while what became a B breeds and stays a B. Maybe later on a couple of A’s breed and have a little baby that looks like neither an A nor a B. Now we have C. B and C or both diverged from A, but B and C are different from one another. They are linked by common, but not direct, descent.


This is a phylogenetic map of the life on Earth. Notice that
we don’t know just what the last common ancestor was, but
you see that eukaryotes diverged from archaea and that
animals, plants, and fungi diverged from protists
(microsporidia, flagellates, ciliates, slime molds) rather
recently. Trees may look a bit different based on what DNA
target gene is being compared.
Scientists use changes in DNA over time to track just when two lines of organisms diverged from their last common ancestor. They can plot this out by time and distance, forming a diagram. This is the study of phylogeny (from Greek phylos = race, and genesis = birth of) and its tools are phylogenetics. Because the diagrams can look like trees, with the common ancestor as the base of the trunk, they are called phylogenetic trees.

A long time ago, a few archaeal descendents had diverged enough to be called protists. They were eukaryotic now, with organelles and special functions, and were starting to think about working together as multicellular organisms. The protists of that time were direct descendents of archaea, but the different protists we know today (see our last few posts here, here, and here) aren’t necessarily directly descended from one another or even from the same archaea.

Some protists diverged from one another. Many stayed as protists, even though they might have evolved to different orders or families over the years. However, others became animals, fungi, or the plants. Our last common ancestor with plants was a protist of some sort, so we have a common ancestor with a pine tree, we just can’t draw a direct line through humans and a pine tree to get to that ancestor.

Let’s use undulipodia (eukaryotic flagella and cilia) to illustrate, or confuse, the situation. We saw that protists – most all of the different protists, use flagella or cilia in one or several ways. Flagella and cilia are characteristics that have been retained in the various descendents of archaea…. But didn’t we also say that prokaryotic flagella and eukaryotic undulopdia are completely different in structure and genes? Yes we did - so what gives.


This is a typical fungus that someone might think of. This is the
basidiomycete mushroom, Phallus indusiatus. Fungi can range
from single cell yeasts (yeah beer!) to hyphal forms that make
your tongue fuzzy, to mushrooms that can take up thousands of
acres. By the way, in New Guinea they worship P. indusiatus as
sacred and that lacy web is called an indusium.
The archaea that diverged to become eukaryotes lost their flagella at some point, and then very quickly evolved them right back again. The structure of the new flagella were different; made from different proteins and having a different structure, but they did about the same job(s).  This re-evolving of a flagellum (and cilium) must have occurred pretty quickly, because all the kingdoms that descended from those early eukaryotes (protists, plants, fungi, animals) have them to some degree or another.

Yet, if you look for undulipodia in the fungal species on Earth today, you’ll find them in only one of the five phyla. Again, what gives? Didn’t we just say that fungi descended from undulipodia containing ancestors?

Four of the phylums of fungus are grouped by characteristics, both genetic and life cycle – the Chytridiomycetes, the Zygomycetes, the Ascomycetes and the Basidiomycetes. The fifth phylum is called the imperfect fungi because we haven’t found a life cycle in them that we can place into one of the other four phyla. But when we do, as we have for some individuals imperfect fungi, they usually fall into the ascomycete or basidiomycete phylum.

However, only chytrid fungi have flagella. Every species in every other phylum of fungi has lost their undulipodia. If you are thinking in terms of phylogenetics – what does this suggest to you?

Yes, very good – the chytrids are probably the common ancestor for all the other fungi. Those that didn’t diverge enough and stayed chytrids retained their undulipodia, but at some point, others lost their flagella and kept on changing into all the other phyla of fungi over time.


Here is a phylogenetic tree of the fungi, showing that flagella
were lost after the other phyla diverged from the
Chytridiomycetes. On the bottom right is a microscopic image
of the mature sporangium of a chytrid fungus. The
zoospores are inside the sporangium. The dark filaments are
rhizobia, not flagella.
You could do the genetics studies to find out which phylum diverged first, and then which one diverged from that and so on, but it would be a waste of time – it’s already been done. The picture to the right shows the phylogenetic tree for four of the phyla of fungi (minus the bothersome imperfect fungi).

What is so different about the chytrids that they kept their flagella, while the others were suited to live without them? There must be something about the chytrids life cycle and/or environment that required the retention of their eukaryotic flagella. Well, they all live in water, maybe they need flagella to swim around. But look at the picture of the chytrid on the right, I don’t see a flagellum anywhere there.

The chytridiomycete name comes from the Greek chytridion, which means little pot.  The pot holds all their zoospores, their reproductive form. It is the zoospores that have the flagella, so they can swim away and establish themselves somewhere with less competition. But that isn’t a good enough explanation. Many water borne fungi come from the basidiomycete or ascomycete phyla, and they don’t have flagella in any of their life cycle stages. Hmmm.

We have tens of thousands of extant (living today) fungal species, and only about 750 or so have any undulipodia. This makes the chytrids exceptional, and is directly related to their being the common ancestor for all the other fungi. If undulipodia are so important that animals, protists, some fungi, and even some plants have them, then why is it that so many fungi seem to get along fine without them? Maybe they’re the exception.

Let’s tell one story of how the chytrid flagella are important. A species of chytrid, called Batrachochytrium dendrobatidis, is responsible for perhaps the largest vertebrate mass extinction in the history of the Earth - and it's going on right now. Most chytrids are sabrophyitc, meaning they eat dead tissue, but a few are parasitic, mostly on plants.


Although the chytrid infection is a large reason for amphibian
collapse, there are others. Mutagens in pollution are responsible
frogs with extra or missing limbs. You can imagine how that
might interfere with long life and mating. It turns out that
amphibians, being in and out of water, are especially vulnerable
to environmental changes.
B. dendrobatidis, on the other hand, is the only known chytrid parasite of living animals - amphibians specifically. The fungi embed themselves in the keratinized skin of amphibians that find themselves in chytrid-contaminated water and then proceed to digest their skin. As many as 6000 species may be vulnerable to this fungus, and several hundred have gone extinct because of it.

You may have heard of the frightening loss of amphibian diversity on the past decades. The reasons for this are known to be several, including toxic pollutants, climate change, and habitat destruction. But B. dendrobatidis has played a significant role as well. Fortunately, a 2011 study showed that a water flea has a voracious appetite for our frog foe and might be used as a control measure. Unfortunately, a 2013 study showed that chytrid-susceptible amphibians may be succumbing to at least two different, and probably more, species of Batrachohytria. So the problem is probably more complex than we thought.

And yes, you read correctly a couple of paragraphs above. Some plants have cells that have flagella. There are moving plants cells! Those will be our exceptions for next week.




Martel, A., Spitzen-van der Sluijs, A., Blooi, M., Bert, W., Ducatelle, R., Fisher, M., Woeltjes, A., Bosman, W., Chiers, K., Bossuyt, F., & Pasmans, F. (2013). Batrachochytrium salamandrivorans sp. nov. causes lethal chytridiomycosis in amphibians Proceedings of the National Academy of Sciences, 110 (38), 15325-15329 DOI: 10.1073/pnas.1307356110

Buck, J., Truong, L., & Blaustein, A. (2011). Predation by zooplankton on Batrachochytrium dendrobatidis: biological control of the deadly amphibian chytrid fungus? Biodiversity and Conservation, 20 (14), 3549-3553 DOI: 10.1007/s10531-011-0147-4




For more information or classroom activities, see:

Common descent –

Fungi –

Amphibian collapse –

Phylogenetics –



Wednesday, April 3, 2013

A Salamander Superhero?

Biology Concepts – primary and secondary toxin, passive and active defense, venom, poison, toxin salamander, newt

Wolverine is a comic book character, as well as a
recurring movie character played by Hugh Jackman.
It’s hard to believe that this is the same man who
played John Valjean in 2012’s Les Miserables. Convict
24601’s tribulations would have been easier if he had
had those claws!
Wolverine from the X-Men is a mammal, but let’s use him as a model for a couple of particular amphibians. Amphibians have developed many different kinds of defenses against predation, but perhaps the most exceptional are found in a certain salamander.

Wolverine had a skeleton that was reinforced with an indestructible metal, could protrude some nasty claws or spines from his hands, and could heal his wounds very quickly. Well, so can Pleurodeles waltl, the Spanish ribbed newt. What is more, our newt friend can go Wolverine one better; P. waltl also produces a toxin and secretes it through its skin!

For clarity sake, P. waltl is actually both a salamander and a newt. All newts are salamanders, but not all salamanders are newts. Salamanders are newts if they fall into one of five genera. In general, newts spend a little more of their lives in or near water, and it is easier to tell male and female newts apart – but there are exceptions in each of these categories.

Egon Heiss at the University of Vienna published a study in 2009 that looked at the unique defense mechanism of P. waltl. It is definitely a poisonous amphibian, secreting a harmful substance primarily from glands at the base of its neck, but from other points along its skin as well. This toxin is noxious and irritating when absorbed through human membranes, but is lethal when injected into mice. And a method of injection is just what P. waltl has evolved.

The ribs of this (and the crocodile newt) amphibian are specially designed and aligned so they can be used as weapons. The ribs themselves are very thick at the proximal end (the end where they attach to the spine), but they taper to points at the distal end. They also have gentle curves downward in the first half, but back up again in the distal half. Each rib is also curved slightly forward.

On X-ray, these look impressive, but they are inside the salamander’s body so they still pose no danger. Beware the secret weapon! When P. waltl is threatened, they go to work. First, the salamander will start to secrete its toxin onto its skin. Then it will assume a hunched posture. By arching its back and holding that position, its rib points actually pierce its own skin and stick out like spines!

Here are pictures from Dr. Heiss’ paper. On the left you
can see the hinge’s on P. waltl’s ribs that allow them to
move to become weapons. You can also see the points
on the ends versus the strong bases to keep them from
breaking. On the right is the posture that P. waltl assumes
to force the rib tips through its skin. The picture only
shows a moderate attempt. They can stick them out
much farther if needed.
The ribs have joints where they meet the spine, and the muscles attached to them pull them forward. The hunching then pulls the skin taut - and here come the sharp points, just like Wolverine.

There are orange spots along the sides of P. waltl that correspond to the points where the ribs protrude, and these themselves are interesting. For some reason, the way the ribs are covered with a connective tissue sheath, and something about the orange spotted skin makes it so the salamander can very quickly heal his self-inflicted wounds - just like Wolverine!

The poison on the skin can be transferred to the wounds created on the would-be predator by the sharp rib points (whether on the skin or in the mouth) allowing the poison to enter the tissues, and making it much more toxic. Does this make P. waltl venomous as well as poisonous? You could argue that point. A venom usually isn’t absorbed through the skin or mucous membranes, but this salamander’s poison is absorbed, so maybe it isn’t a classic venom. But it is a toxin that uses a natural delivery system to enter the tissues of the victim like a venom, so the argument is on.

We can use P. waltl to discuss a larger issue in poisonous amphibians. As a salamander, not much is known about where its poison comes from. He may take the poison from the food he eats, whether it be plant or insect, or he might produce the toxins through his own biochemistry.

I talked to Dr. Heiss about this issue in P. waltl. He said that he has raised eight generations of the spine ribbed salamanders in the lab, feeding them very non-toxic diets. Yet, he has been stuck in the finger by a rib and this finger swelled and stung much like a bee sting. He takes this as anecdotal evidence that P. waltl makes its own toxin.

The blue-ringed octopus is one of the most deadly
animals in the seas. It lives in the shallow coastal
waters off Australia and Indonesia. Its venom is a
secondary toxin. In 1989 it was suggested that
several bacteria might be producing the toxin in the
octopus' salivary glands. This same toxin is taken
up by many very different animals, like octopuses,
pufferfish, newts, and snails, so the idea that is
produced by something else is logical.
There is a possibility that P. waltl still sequesters toxin despite his non-toxic environment. Many animals, like the blue-ringed octopus, use toxins that are produced by microbes on, in, or around their bodies. Even if fed a non-toxic diet, if P. waltl harbors a bacterium that makes toxin and P. waltl passes that bacterium vertically to its offspring, it could be a source of newt toxin even in the laboratory environment.

Much more is known about poisonous frogs. Poison dart and other poisonous frogs gather their toxins from the food they eat, mostly poisonous beetles, ants, and especially poisonous orbatid mites. They then sequester the toxins in glands on their backs or elsewhere on their skin. As these frogs don't make their own poisons, the toxins are called secondary toxins.

Most poisonous frogs sequester toxins from their prey, but not all. Frogs of the genus Pseudophryne (like the Corroboree Frog of Australia) make their own toxin in addition to sequestering toxins from their diet. Dr. Alan Savitzky at Utah State University told me that diet does play a role, as the pseudophryne frogs make toxin themselves only when their toxin-producing prey is not available. This saves ATP; making toxin is a waste of energy when it is readily available from the environment.

Other amphibians, like most poisonous toads, use primary toxins, meaning that they produce them by their own physiology. True toads (family Bufonidae) commonly make a toxin called bufadienolide inside skin glands; the starting molecule they use is cholesterol. Too much cholesterol can kill you in several ways!

Cane toads are not native to Australia in 1935
from Hawaii to try and control the sugar cane
beetle. That’s weird, most times, it is things
introduced TO Hawaii that cause problems, not
FROM Hawaii. It isn’t too strange to think a cane
toad cold kill a crocodile when you realize that
an adult cane toad can weigh 2kg (4.5 lb)!
Cane toads introduced into Australia are a classic example of bufotoxins at work. The toads have killed thousands of native animals that have eaten them, so scientists are putting out sausages made with a little bit of cane toad poison, in an effort to teach native animals not to eat the toads.

However, the exception to primary toxins in toads is in the genus Mealnophrynicus. These toads make toxin, but they also sequester toxin, much like the pseudophryne frogs. These sequestering and toxin producing exceptions are discussed in the wider context of sequestered toxins in Dr. Savitzky's great 2012 review paper in Chemoecology.

Some animals are smart to use the toxins of their prey - some poisonous frogs are even smarter; they add their own biochemistry to the toxins they steal. Take some dendrobatid frogs for example. They aren't satisfied with merely using the toxin they sequester, they make it more potent by changing it's chemistry.  They can hydroxylate a dietary toxin called pumiliotoxin to become allopumiliotoxin. The allo-version is about 5x more toxic than the version they eat!

So, is this modified toxin a secondary toxin, or has it crossed over into being a primary toxin? So much is grey area. Let’s pile on another exception. In some cases, toxins that an animal eats are spread throughout is body, either in a biologic effort to make its tissues toxic, or just because they have not been broken down by the body yet. This is called toxin retention, and is a separate mechanism from toxin sequestration in glands specifically designed to concentrate the consumed toxins.

Here you can see the toxin from R. guttatus being squirted
out of a gland on its back. This is a unique activity for
toads (as far as we know), but there is a salamander
that can do it too. I guess nothing in biology is 100% true,
and nothing is unique to a single organism. The picture is
from Dr. Carlos Jared’s 2011 paper.
Primary and secondary poisons secreted on the skin are usually considered passive defenses. They only go into action when the animal is bitten. Predators usually learn quickly to avoid that kind of animal – if they aren’t already dead. This is why poisonous frogs are often colorful, it helps the predators recognize them as something bad to eat. This kind of defense is the opposite of camouflage, and is called aposematism.


Poisonous toads usually have a passive defense, even if some of their toxins are lethal, but there is an exception - wouldn't you know it. The Amazonian toad Rhaebo guttatus can become more active in use of its primary toxin. R. guttatus can voluntarily squirt its toxin from the glands on its back, and can aim it at a predator! This defense was described in 2011 by Carlos Jared and his team in Brazil, even though the toad was first discovered over 200 years ago! The toad inflates its lungs, creating pressure in the skin on its back, and expelling the toxin. The direction is based on subtle movements of the toad's skeleton and musculature.

This leads to a final point that reminds us how much communication plays a role in science, and how it is a group activity. When looking for exceptions in amphibian toxins, I kept coming across papers about “toad venom,” but when I read the papers, they were really talking about toad toxin; they were never delivered below the skin.

I starting asking scientists why this might be, and I got several answers. Some tried to make an argument that venom just means that it is sequestered in glands – I reject this argument. Dr. Savitzky said that many scientists are guilty of using the term incorrectly, but it persists because of “cultural inertia.” I buy this explanation – I think it explains other weird occurrences, like Justin Bieber’s popularity.

Here is a recent scientific paper that uses the phrase “toad venom.” I did 
a computer search in the best medical research database there is, 
and “toad venom was used 88 times, while “toad toxin” was used 
only seven. Even more illustrative, a search for both words toads + 
venom showed 4500 papers, but toad + toxin, only 350. Misuse of the 
of the phrase is rampant, even in the people who study them!
Finally, Dr. Carlos Jared pointed out that in the latin-based languages of Portuguese and Spanish, the words venom and toxin mean exactly the opposite of what they mean in English. It is easy to see then how a term like “toad venom” could become ingrained even in the scientific literature. Warning – be precise in your language, or you could be the source of an unfortunate mess.

Next week, talk about some weird examples of venom in snakes; or are they poisons - if you spit it, is it still a venom?


Savitzky, A., Mori, A., Hutchinson, D., Saporito, R., Burghardt, G., Lillywhite, H., & Meinwald, J. (2012). Sequestered defensive toxins in tetrapod vertebrates: principles, patterns, and prospects for future studies Chemoecology, 22 (3), 141-158 DOI: 10.1007/s00049-012-0112-z

Heiss, E., Natchev, N., Salaberger, D., Gumpenberger, M., Rabanser, A., & Weisgram, J. (2010). Hurt yourself to hurt your enemy: new insights on the function of the bizarre antipredator mechanism in the salamandrid Journal of Zoology, 280 (2), 156-162 DOI: 10.1111/j.1469-7998.2009.00631.x

Trefaut Rodrigues, M., Felipe Toledo, L., Kruth Verdade, V., Maria Antoniazzi, M., & Jared, C. (2011). The Amazonian toad Rhaebo guttatus is able to voluntarily squirt poison from the paratoid macroglands Amphibia-Reptilia, 32 (4), 546-549 DOI: 10.1163/156853811X603724



For more information, see:

Spiny-ribbed salamanders –

Cane toads –

Aposematism –
http://en.wikipedia.org/wiki/Batesian_mimicry