Wednesday, October 15, 2014

Frankenstein Meets Genetic Modification

Biology concepts – Frankenstein, asystole, ethics, genetically modified organisms, genetically modified foods, synthetic biology, decomposers, electroconvulsive therapy

Mary Shelly was wedded to Percy and friend to Lord
Byron, one of the great poets of the early 19th century.
But she was a fair writer on her own. Note the bolts on the
monster's neck. These were added by make-up artist Jack
P. Pierce. He said they were electrodes, not bolts, even
though Mary Shelly never actually wrote that
the good doctor used electrodes on the body.
Can you think of anything scarier for Halloween than an irresponsible scientist letting his creation loose on the world? Now imagine that his creation is something that violates our sense of decency and our reverence for the dead. Well, that’s the story behind Mary Shelly’s Frankenstein.

Who's the victim of the story? Is it Dr. Frankenstein, who’s family is murdered or is it perhaps his monster, who was brought into the world and abandoned? He lives his second life shunned by all, misunderstood, lonely, unable to live with dignity or even die at all.

This is a big story for a 17 year old to pen. Yep, that’s how old Mary Shelly was when she wrote Frankenstein (published when she was 21 in 1818). Despite her age and inexperience, she rolled out one of the greatest novels ever. It was both romantic and a criticism of romance. It sparked the science fiction genre and was the beginning of horror stories.

The movies and stories about Frankenstein’s monster usually highlight the way in which the monster was created and his ugliness and hatred, but that isn’t what the book is about. It’s a story of responsibility in science and toward others.

The Age of Enlightenment had just ended when Frankenstein was written, and the Romantic period was in full bloom. A switch from science to emotion meant that the facts and discoveries about the world now needed to be examined, not just accepted. Here was Mary found her message – a person must be responsible for the things he/she creates – be they physical things, knowledge, or opinion.

Electrical impulses make muscles move. Adding salt to
freshly skinned frog legs is a lot like hitting the with a
mild jolt of electricity. This is like Galvani demonstrated
with the corpse of the murderer and the image Mary
Shelly evoked in her novella.
The science of the monster’s reanimation was not the focus, but Mary had good knowledge of the latest science of the day, and this is what informed her making of the monster. Sir Humphrey Davy of the Royal Institution of Science had just stated that chemistry would, eventually, control the conversion of dead matter into living matter.

This was combined with the advances in electricity at the time. Just before 1800, Luigi Galvani had published on the ability of electricity to excite the muscles of dead animals – the innate electrical force of living tissue came to be known as “galvanism.” In 1803, Galvani applied an electrical charge to the corpse of executed murderer Thomas Forster, and the body jolted and moved – a good visual for Mary.

So could a body be reanimated as Shelly relates in the novel? Nope…. at least, not yet. Let’s examine why.

Dr. Frankenstein uses a corpse, with some implied modifications through surgery. Not good. Immediately after death, cells that are starved for oxygen stop making ATP. ATP is required to maintain lipid membrane compartments and in general for the integrity of the cell. Once there is no oxygen and no flow of energy, the enzymes designed to break down wastes, toxins, and old organelles for recycling are released to the cytoplasm and start to destroy the cell.

Consider the process of rigor mortis. Muscle contraction requires ATP not to contract, but to release the contraction (see this post). With no ATP, the muscles become rigid in their contraction about 3-4 hours after death. Rigor lasts for about 12-20 hours, and is only released by the process of cell destruction that we described above.

Frankenstein’s monster better have been a very fresh
corpse. Decomposers like bacteria and fungi are already
in and on your body; it’s your immune system that keeps
them at bay. Once dead, we’re all just food for worms,
prokaryotes, protists , fungi, and of course buzzards.
Mary doesn’t describe anything to overcome this problem. But there are other problems as well. No life, no immune system. This is what keeps our fungal, bacterial, and protist flora in check. Without a working immune system, the microorganisms that are normally growing in and on us will be unchecked and start to grow and feed on the corpse. This is where they get their name, “decomposers.” Mary doesn’t mention anyway to overcome that problem either.

What about the electrical problem? We use electricity in our neural system and in our heart. Your brain is an electrochemical machine, using ions to generate and electrical current down axons. Electroconvulsive therapy (ECT) is useful in treating some forms of depression and schizophrenia and mania, but we don’t really know how it works yet.

Several hypotheses exist; none or all of which may be correct. ECT may alter neurotransmitter concentrations, which would change the degree to which impulses are transferred or suppressed from one neuron to another. It may work to prune back some neural connections in the brain, or it may work to stimulate hormone release that could alter the brain chemistry. A 2014 review provides more information on the various theories of ECT mechanism.

From top to bottom we see a normal heart rhythm, and a
then a ventricular fibrillation that CAN be treated with
electric shock. Below that is a pulseless rhythm, which
looks normal but doesn’t move the heart, and then asystole,
with no pulse at all. The bottom two CANNOT be treated by
shocking the heart. That’s why they called it a defibrillator,
not a heart starter.
Electricity is used in the heart as well. We can modulate the rhythm of the heartbeat with a pacemaker, which is just a low voltage shocking device. When a person is dying from a poor heart rhythm (ventricular tachycardia or fibrillation), we can use a defibrillator to shock the heart back toward a normal rhythm.

Mary’s error: electrical shock won’t start a stopped heart (called asystole, a = not, and systole = contraction), despite what you’ve seen on the TV shows. For asystole, the treatment is CPR with a shockingly large dose of adrenaline every 5 minutes.

Dr. Frankenstein couldn’t have reanimated his self-digesting, microbiological dinner plate of a corpse with an electric shock, but if the muscles hadn’t gone into rigor yet, he might have been able to get a short slam dance out of him. But then, this isn’t really the point of the story.

Frankenstein’s monster was alive and wandering the world alone a mere 1/5 of the way through the story, so it’s really a story of how to deal with the products of science. Erasmus Darwin (Charles’ grandfather) had introduced the idea of mutations or “monstrosities” being passed on or inherited – so Mary now had the essence of the story. Who is the monstrosity - the monster or the scientist who creates and then abandons it?

Erasmus Darwin was Charles granddad. He was an
inventor, poet, natural philosopher and I hear a great
cook. One of his poems predicted the discovery of the
Big Bang, he also suggested the idea of natural
selection and mutation and sketched out a liquid
oxygen and hydrogen rocket.
One indication that a story is a classic is whether its themes are applicable in different eras. Frankenstein may be even more applicable to our times than it was to Mary’s. Current debates are boiling over concerning the uses and limitations of science.

The issue most often compared to Frankenstein’s monster is genetically modified organisms (GMOs). Have you heard the term, “Frankenfoods?” This is the name that opponents of GMOs and particularly GM foods use to taint the agricultural biotechnology industry.

The fear is that by tampering with nature and introducing genes into organisms, we are creating monsters that might have unexpected effects on us. It’s a good marketing campaign idea, and it has stuck in the minds of the public.

Europe and Russia have banned all GM foods out of fears that they may contain toxins or mutagens that would harm the consumers. One fear is that DNA from the genetically modified organisms would be transferred to the eater and combine with their own DNA. That is a scary sounding idea.

The problem is, you take up DNA from the food you eat every day, although not whole genes as the fear warrants. Digestion breaks down DNA, so we take up mostly nucleotides and short stretches of nucleic acid. No recorded evidence exists of uptake of an entire gene.

Dr. Frankenstein used all natural body parts, no artificial
sweeteners, additives or preservatives, and good old-
fashioned electricity. If he was sold in the market, the
monster could be labeled as organic! No genetic
modification here.
Websites and books talk about the dangers of GM foods, but the evidence hasn’t shown up in the scientific literature. What few papers have announced negative ramifications of GM foods have been retracted or have such vague conclusions as to apply to any food at all. I’ll give a typical example.

In 2012, a researcher named Seralini from the U. of Caen announced that an herbicide used with GM foods (glyphosate in Roundup) causes tumors. He didn’t just publish it, he had a press conference and concurrent release of his book on the subject and videos in three different languages. It turns out that he also had a company that was preparing to market a product as a “protectant” against glyphosate. The study was subsequently retracted, but a modified version with a conclusion that “more study is needed” was re-published in a lesser journal (see note below).

Other studies on the dangers of GM foods have been correlative, meaning that when you see “A”, you often see “B.” But that doesn’t mean that A causes B, or that B causes A. Remember this: correlation does not imply causation.

The truth is, we need more studies. There are real issues to be dealt with, such as - does introduction of a particular gene cause plant toxins to be increased – this could be bad for us. The idea is the same as in Mary Shelly book – we must be responsible for those things we make. No GMO or GM food should go to market without extensive testing.

The testing to date shows that there are no health risks associated with GM foods. Longitudinal studies from 2014, 2013, and 2012 of live stock feeds showed that animals fed GM crops over five generations showed no ill health effects and their meat was exactly like that of animals fed conventional feed. By the middle of 2013, over 600 studies showing that GM foods carried no health risks had been peer-reviewed and published. The key is always the same - responsible and thorough testing.

Synthetic biology has arrived. Vanilla is a very expensive
crop to produce. But a gene has been constructed and
vanillin is now produced in yeast. They ferment sugar and
produce vanillin. This is more natural than artificial vanilla,
and contains many of the metabolites that make vanilla
taste like vanilla.
The problem of hidden agendas like Seralina's does go both ways; a 2014 editorial on the safety of GM foods was written by a Monsanto employee, the company that markets GM corn and soybeans. Society must be diligent and demand topnotch, transparent, and responsible science. This was one of Shelly’s themes, Frankenstein conducted his work in private, with no comment from society about how or whether it should be done at all.

The next generation of people will have more issues to deal with, like synthetic biology (not merely taking a gene from one organism and putting it another, but constructing a gene or genes from nucleotides and then inserting them). How to ensure good use of science? - transparent methods and results, no hidden agendas, no jumping to conclusions, and a very science literate population that can judge and reason for themselves. And that’s why we learn biology.

Next week - Halloween is a time to focus on what's scary and what's dead. Can you actually be scared to death?

The retraction of the 2012 study of Seralini in Food and Chemical Toxicology can be found here. It was republished in modified form in the journal, Environmental Sciences Europe in 2014, but with no peer-review.

Goldstein, D. (2014). Tempest in a Tea Pot: How did the Public Conversation on Genetically Modified Crops Drift so far from the Facts? Journal of Medical Toxicology, 10 (2), 194-201 DOI: 10.1007/s13181-014-0402-7

Tufarelli V, & Laudadio V (2013). Genetically Modified Feeds in Poultry Diet: Safety, Performance and Product Quality. Critical reviews in food science and nutrition PMID: 24915369

Van Eenennaam AL, & Young AE (2014). Prevalence and impacts of genetically engineered feedstuffs on livestock populations. Journal of animal science, 92 (10), 4255-78 PMID: 25184846

Snell C, Bernheim A, Bergé JB, Kuntz M, Pascal G, Paris A, & Ricroch AE (2012). Assessment of the health impact of GM plant diets in long-term and multigenerational animal feeding trials: a literature review. Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association, 50 (3-4), 1134-48 PMID: 22155268

McCall WV, Andrade C, & Sienaert P (2014). Searching for the mechanism(s) of ECT's therapeutic effect. The journal of ECT, 30 (2), 87-9 PMID: 24755719

For more information or classroom activities, see:

Genetically modified organisms/foods –

Wednesday, October 8, 2014

A Tale Of Two Tails

Biology concepts – flagella, bacteria, prokaryotes, eukaryotes, undulipodia, axoneme, basal body, centriole

Everyone has the dream where you show up for a class
that you didn’t know was on your schedule, only to be
having a test. But in second place is the dream where you
are back in elementary school, or maybe the principal’s
office. Above is a picture of every teacher I had in
elementary school.
You find yourself transported back to sixth grade grammar class. You barely fit in the desk and your clothes are out of style.... again. You don’t know how you got there, but the immediate problem is that Mrs. Belcher has just called your name to answer the next question. What are homonyms?! You stare back at her with terror in your eyes.

But your study of word roots may help you survive. Homo- means same, while -nym means word. OK, it’s coming back to you. Homonyms can be words that are spelled but have different meanings and origins (called homographs) or words that are pronounced the same but have different spellings and meanings (called homophones).  Yes! The class cheers, and Mrs. Belcher is more than mildly surprised. Crisis averted.

I have no idea how you got transported back to grammar school, but your question and answer is very timely to our discussion today. Homographs, like minute (min-it, a short time) and minute (my-noot, a small amount), look the same, but have different meanings. Homophones, like to, too, and two sound the same but mean different things and have different origins.  This is very much like the differences in prokaryotic flagella and eukaryotic undulipodia. Too much of a stretch for you... maybe.

We have seen that bacterial flagella are long, whip-like structures protruding from the cell that can aid in motility. So are eukaryotic undulipodia. They look very similar, yet we are going to see they have very different structures, mechanisms of function, and origins – just like homophone and homonyms.  So maybe the analogy wasn’t so far off.

Both flagella and undulipodia extend from the cell surface with a long tail. But in the prokaryote, this was made of small subunits of flagellin proteins. In the undulipodia, the structure is called the axoneme, and is made of long microtubules of tubulin protein. Already we have significant differences between two things that look very similar.

A cross section of an undulipodium axoneme looks like
this – although I’m not sure they’re color coded in the
cell. Notice how the inner are connects the nested tubule
of one doublet to the outside tubule of the next doublet.
The inner arms are responsible for the degree of bend,
the outer arms are involved in the rate of movement. There
are other proteins involved, but we aren’t getting that
detailed. Maybe you want to do that on your own.
The axoneme (axo = axis, and neme = thread) of the undulipodia has a very distinct structure which is best appreciated when you look at it in cross section. The long microtubles appear as small circles in the cross cut, but they are arranged very precisely (see picture). They come in doublets, and there are nine sets of them surrounding a central doublet (called 9 + 2 or 9(2) + 2). This is very different from the single hollow tube of the prokaryotic flagellum.

The way the axoneme is built is also the key to how it works. The different microtubule doublets are cross-linked by protein complexes called dynein arms. There are inner arms and outer arms. An inner arm connects one microtubule from one doublet to another microtubule of the adjacent doublet. When one doublet slides further out from the cell body and the connected adjacent doublet doesn’t, this creates stress and the whole thing must bend to maintain the connections.

So, walking proteins are how the undulipodia create their whip-like action. There is a walking system analogous to dynein arm movement that has developed in many animals. We have looked at muscle contraction before. Just like myosin heads walking along actin filaments that are anchored to the muscle cell membrane, the dynein arms on some doublets start to crawl up or down the adjacent microtubule of an undulipodia creating a bend and then they can reverse to whip back the other direction. This is very different from the spinning motor of the bacterial flagellum.

Pay attention to these cartoons, they show how the undulipodia
bend. ATP powers the sliding of the dynein arms. As they move
down one tubule, that filament moves up. If the filaments are
anchored in the membrane, as they are in undulipodia, the
movement creates tension and a bend. The cartoon on the
right is a good summary.
The motions the two different mechanisms produce is different too (a homophone). While the prokaryotic flagellum spins like a propeller, the sliding of the microtubules makes the undulipodium wave back and forth, like a field of wheat on a breezy day, or how a snake might thrash if you held his head down (don’t just hold his tail down, he’ll bite you).

The undulipodium motion often occurs in just one plane, back and forth instead of all around, but that doesn’t mean it has too limit itself to that. It can spin too; it just takes a very coordinated sliding back and forth of microtubules.

Another difference between prokaryotic flagella and eukaryotic undulipodia is in how they are powered. We saw that flagella in bacteria get their force from the spinning motor, and the motor gets its energy from an ion gradient across the membrane. But in eukaryotes, it was seen early on that if you strip the membrane off of an undulipodium, and added ATP, they start to move.

Yes, all undulipodia are held within the membrane. Some bacterial flagella are membrane covered, but all eukaryotic versions are sheathed in plasma membrane. But back to the ATP. Exposing the naked undulipodium to ATP, even on a dead cell, can initiate the dynein walking and microtubule sliding, so it is definitely ATP powered.

Also, this points out that the power for the bacteria movement comes from the motor in the base, but the eukaryotic movement is in the axoneme, not the base. The basal body that anchors the eukaryotic undulipodium into the cell membrane is amazing in its own way. The basal body is actually a centriole, the same structure that helps to move the chromosomes apart in the spindle apparatus during mitosis. We’ll come back to this double duty organelle in a a few weeks.

Chlamydomonas algae species have a double flagella
for swimming. A single stroke as shown above. The
power strokes on top is followed by the recovery stroke
below. Put all the numbers together and looks like
someone swimming underwater. The picture of the
organism is there because it’s always better to see the
real thing as compared to a cartoon.
Our two systems still look similar, but we see how they are not so similar in structure and action. Since eukaryotic cells are so much bigger than prokaryotes, the first flagella to be examined and found to have the 9(2) + 2 structure were in sperm tails.

But soon after that, the protozoans were discovered to have undulipodia as well. Organisms from the algae genus Chlamydomonas have two long undulipodia that they use for motility. Located at the front of the cell, their movement pulls the alga through the water. But protozoans are just as likely to have undulipodia that push them through water. They can work both ways.

Amazingly, when a Chlamydomonas finds itself out of water, the undulipodia resorb in short order. Nature hates to waste energy, so why maintain a boat motor if you’re not in the water. But place them back in a liquid environment and the two structures will reassemble with in an hour – with the same structure 9(2) + 2 and working the same exact way.

Of course, saying they all have the same 9(2) + 2 structure is an invitation to find exceptions, and science has found them. A 2006 study found that rabbits are quite the rule breakers. Sure, they have 9(2) + 2 axonemes, but they don’t stop there. Some rabbit embryo undulipodia show a 9(2) + 0 structure, where the central doublet is completely missing, yet the structure functions just as other motile undulipodia.

What’s more, rabbits can also have 9(2) + 4 axonemes, with double the number of central microtubules. Again, they function just fine. Is there a reason for these variations – maybe, but maybe they are just mutations that didn’t have a negative impact, so they were retained.

You know how annoying it is when you touch a cactus
and those little bristles get stuck in your skin? Well,
don’t touch a bristleworm. They’re lined with those painful
bristles – hence the name. Somebody studied these worms,
and found out they have parasitic protozoans in their gut.
Then someone studied those parasites and found that they
have sperm. And someone studied the sperm and found
that they have unique axoneme structures. I love science.
A couple of parasitic protozoans that live in bristle worm guts show differences in their axonemes. Lecudina tuzetae sperm tails have a 6(2) + 0 structure, while the Diplauxis hatti protozoan sperm has a 3(2) + 0 axoneme. Described in a 1980 paper, this is the simplest motile undulipodium known – as of now.

The undulipodium basal body (born as a centriole) can have exceptions as well. The vast majority have a structure of 9(3) + 0, where instead of doublets, they have triplets. This makes sense since they need to be strong to support the axoneme.

But diatoms, very small algae cells protected by a silica shell, can have sperm that look very different, according to a 2013 study. Their basal bodies have been observed to have doublet microtubules, and are very similar to the axoneme. Even weirder, a couple of insects feel the need to go big with their basal bodies. Acerentomonon microrhinus, a primitive hexapod insect has sperm tail basal bodies with 14 microtubule doublets, while Sciara coprophila, a fungus gnat (see picture), has up to 90 singlet microtubules in its sperm basal body.

We have talked a lot about sperm tails and protozoan motility structures, and these undulipodia look the most like bacterial flagella. But undulipodia come in a couple of flavors; those longer than 40 m or so are called flagella while the shorter ones are called cilia. See the naming problem and why Lynn Margulis came up with undulipodia?

This is a fungus gnat – it sounds like they eat fungus,
but nope. Only the larval form feeds; the adults never
eat. That’s OK, they don’t live very long at all. They
overwinter in their adult form because they are unique
in that they can both tolerate freezing weather and freeze
themselves without damage. It must be important, since
their sperm tails are loaded with 90 microtubules in the
basal body – everyone knows that massive numbers of
microtubules is the best way to avoid cold damage.
Both eukaryotic flagella and cilia have the microtubule and dynein arm structure, with centrioles for their basal bodies. There are exceptions to the cilia that we will look at in a few weeks, but the biggest difference between them, besides their length, is that cilia occur in groups, while flagella are usually found in ones or twos. You could say that cilia and flagella are like synonyms, they have almost the same meaning (and structure), although they are two different things.

Next week – Halloween is coming, so what better time to have a discussion of genetically modified foods and an 19th century teenage girl who wrote the best science fiction book ever.

Prensier, G., Vivier, E., Goldstein, S., & Schrevel, J. (1980). Motile flagellum with a "3 + 0" ultrastructure Science, 207 (4438), 1493-1494 DOI: 10.1126/science.7189065

Idei, M., Osada, K., Sato, S., Nakayama, T., Nagumo, T., & Mann, D. (2012). Sperm ultrastructure in the diatoms Melosira and Thalassiosira and the significance of the 9 + 0 configuration Protoplasma, 250 (4), 833-850 DOI: 10.1007/s00709-012-0465-8

Feistel K, & Blum M (2006). Three types of cilia including a novel 9+4 axoneme on the notochordal plate of the rabbit embryo. Developmental dynamics : an official publication of the American Association of Anatomists, 235 (12), 3348-58 PMID: 17061268

For more information or classroom activities, see:

Undulipodia –

Wednesday, October 1, 2014

One Thing Is Just Like The Other – Sort Of

Biology concepts – undulipodia, convergent evolution, parallel evolution, homologous structures, re-emergent evolution, atavism, flagella, eukaryote, prokaryote

This represents the evolution of cell phones over the last
couple of decades. The latest models aren’t there since
things are changing so fast. Evolution in biology doesn’t
always work this way, one thing leading directly to another,
sometimes you have to go back to a rotary phone go forward
to an iPhone, and sometimes two phones (species) will look
exactly alike although they were designed in secret by
different companies.
Two things look similar and perform the same function. Chances are, they have the same origin; one got copied from, or spawned, the other – see the phones to the right. Evolution in technology makes sense, but it’s not always so simple in biology.

Let’s use our flagellar example from the last few posts. Prokaryotes have flagella and use them for motility, amongst other things. Well, some eukaryotic cells have flagella too. Eukaryotic cells evolved from archaea that swallowed bacteria (see this post), so it makes sense that eukaryotic flagella evolved from prokaryotic flagella. But all evidence says no.

We’ll get into this more in the coming weeks, but flagella and similar structures in eukaryotes have very little in common with flagella from prokaryotes. Eukaryotic flagella are made up of a ring of microtubules surrounding a core of microtubules. Microtubules have nothing to do with bacterial flagella, since they are made up of polymers of flagellin protein with a hollow core, as we have discussed.

These cartoons show the differences between the
prokaryotic flagellum (left) and the eukaryotic flagellum
(right). They look pretty similar from afar, but their
structures are completely different. What you can’t see
are the genes that code for these. There are NO similarities
between the genes for the prokaryotic
and eukaryotic flagella.
Likewise, the base of the prokaryotic flagella is a series of rings that anchor it into the membranes and wall, and the motor spins in one direction and then the other based on movement of ions across a gradient. But eukaryotic flagella have a base that is not involved in the movement, yet is important enough to be derived from another organelle.

If eukaryotic flagella had evolved directly from prokaryotic flagella, then they would be termed homologous structures, having similar function and similar structure because one is directly descended from the other. There might be small or large adaptations that change the genes, structure, or function a bit, but there is still a direct link from one to the other.

Examples of homologous structures are the forelimbs of larger animals. The arm of a human, the forelimb and paw of a cat, the pectoral fin of a dolphin and the wing of a bat. They all have similar structure and function and they come from a common ancestor; they’re all mammals.

Direct descent with adaptation is how evolution works most often. But flagella in eukaryotes and prokaryotes aren’t connected by common genes or structures and you have to go so far back for a common ancestor. This is one of the exceptions – an exception called convergent evolution.

Convergent evolution is defined as independent evolution of similar features in species of different lineages. It produces analogous structures – they may look the same and function the same, but were derived separately. An example would be flight. Flying insects, birds, and bats all developed flight and they all use wings, but wings developed for each after their ancestors split away from one another.

You don’t have to be a specialist in dermatoglyphics (fingerprint
analysis) to see that koala prints are very similar to human.
They have to grasp tree limbs and we have to grasp beer
bottles –it’s about the same thing. However, koalas only have
ridges on their fingertips, toetips, and selected parts of their
palms and soles, not like humans that have them all over the
working sides of our hands and feet.
A better and weirder example of convergent evolution to analogous structure has occurred between koalas and primates. I’d say we diverged more than 100 million years ago, yet primates and koala bears of Australia have almost indistinguishable fingerprints.

Friction ridges, or dermal ridges, are better names for fingerprints and they give a clue as to their function. The ridges help gain and maintain grip. The fingerprints of gorillas and chimps are pretty similar to humans; they're unique but don’t follow the same frequency of types as human prints.

However, a 2012 study in a forensic science text funded partially by the FBI, showed that Koala prints are almost indistinguishable from those of humans. In fact, in an interview with the author, he said that his fingerprint technician failed to pick out the human print when given a koala print and a human one to compare. Next time a crime is committed, the police will have to suspect all the koalas without alibis.

We can compare convergent evolution to another mechanism - parallel evolution. In this exception, two lineages start with similar traits because of common ancestry. Over generations they each change, but the structures and function still remain similar. This is different from convergent evolution where two different traits become more similar.

The top cat (not topcat) is Smilodon, a placental mammal that
lived in North America from 2.5 million years ago until about
10,000 years ago. On the bottom is the Thylacosmilus, a marsupial
that died out in South America a couple of million years after the
Smilodon arose. If that isn’t an argument for parallel evolution,
I don’t know what is.
A classic example of parallel evolution is between species of marsupial and placental mammals. They diverged while living in the same places at the same time, so they could each fill some empty niche. But then the continents divided. In Australia, the marsupials predominated, while in Europe and Asia the placental animals won out. In South America, they have both remained.

When the dinosaurs disappeared 65 million years ago, many niches were open and the mammals took off, becoming more numerous and more diverse in all areas. Then we saw the parallelism. In Europe, we had the smilodon (saber-toothed cat) and in South America we had the Thylacosmilus – a saber-toothed marsupial. They looked remarkably similar. In Tasmania, a marsupial wolf developed, while in Europe and North America, it is the placental wolf. All were separated by reproductive mechanism and geography, but showed parallel evolution.

Convergent evolution usually refers to things that weren’t present in their last common ancestor, but prokaryotes already had flagella when eukaryotes diverged. This is a quandary. Parallel evolution sounds a little more like it might apply to bacteria versus eukaryotic flagella – they have a common ancestor, although you have to go way back, and they have developed remarkably similar functional structures. Think about all the different possibilities of motility, and yet they both developed a whip? Seems impossible that they couldn’t be related somehow.

But then again, parallel evolution doesn’t make sense because prokaryotic flagella are built completely different from eukaryotic flagella. Why don’t eukaryotic flagellar genes and parts mimic those of prokaryotes if they came from a common ancestor? They look similar and function similar, yet are built completely differently.

Atavisms like a human vestigial tail do occur. This is a system
that had been turned off du to regulatory genes, but sometimes
they don’t work completely. However, many pictures of supposed
tails are actually cases of spina bifida, an incomplete closing of
the spinal column. The picture on the right – see the bones in the
tail? Definitely not spina bifida.
Maybe the eukaryotic flagellum is an atavism (at = beyond, and avus = grandfather), a trait that got turned off. Many generations didn’t display it but the genes were still there. Then the feature was pulled back out of the gene pool when it was needed again, or sometimes without being needed.

For example, humans have a common ancestor with tailed mammals. Every once in a while, gene regulation gets fouled up in utero and a baby is born with a vestigial tail. The genes were still there to make a tail, they were just hidden by the ways the genes are regulated – who gets to be turned on or off. The whole tail isn’t there, but enough to see that the blueprint is still in our DNA. This is an atavism. But this isn’t what happened with flagella, because the genes are so different from prokaryotes to eukaryotes.

What we have with flagella is most likely a case of re-evolved convergent evolution. The trait was lost and then evolved again. It isn’t unheard of to lose traits via evolution. It happens all the time.  It isn’t efficient, but nobody said evolution was efficient. That’s not evolution’s aim; it doesn’t have an aim. Nature reacts to mutations, pressures, and environments from generation to generation. Evolution is not a straight line.

It's more common to lose a trait than it is to re-evolve one. A study from 2009 cited the idea of relaxed selection, when a trait becomes useless after once being beneficial. Fish that become cave dwellers don’t need eyes, so they disappear over generations.

A less common example would be if a prey animal suddenly finds itself without predators. Over a short number of generations the prey animals become less alert and slower because those traits are needed any more. In general, the more costly a trait is to maintain, the faster it will be lost when selection is relaxed.

Relaxed selection is the idea that traits not needed can be lost. If t
he lion chooses not hunt the zebra any longer (he heard that
they’re high in cholesterol), then they could lose their stripes
because they don’t need to hide, they could become bigger since
they don’t to be so fleet of foot, and they could become less easily
startled. They might even choose to live alone.
On the other end of the scale, a 2011study in frogs showed that they lost mandibular teeth 230 million years but were able to re-evolve them about 5 million years ago.  This violates something called Dollo’s Law of Irreversibility, which states that when a trait is lost, it can’t be regained. Oops, maybe that law should be taken off the books. Maybe they mean that it can’t be duplicated exactly. I’m sure that the gene sequence and shape of the new mandibular teeth is at least slightly different from the originals.

Wings, the example we gave above as convergent evolution, are another example of re-emergent evolution. According to a 2003 study of stick insects, the woody little buggers have evolved, lost, and re-evolved wings several times.

The final nail in the coffin of common ancestry for prokaryotic and bacterial flagella is that the eukaryotic versions are closely related and structured exactly like another eukaryotic feature, the cilium (plural cilia, from Latin for eyelash). Prokaryotes don’t have cilia, but they’re found all over the eukaryotic world.

The similar structure of cilia and eukaryotic flagella shows that they are commonly descended - they are truly homologous structures – many cells even have both. The problem comes when you try to talk about them and still separate what your saying about eukaryotes from the prokaryotes.

Lynn Margulis (1938-2011) was a daring biologist.
She stood by her guns with several controversial
hypotheses, and most often shown to be close, if not
right on the money. Maybe it wasn’t so odd that she
thought big thoughts, she entered the University of
Chicago at age 14, she was married to astronomer
Carl Sagan, one sister married a Nobel Prize winner
in physics and the other married a mathematician, her
sons and daughter are authors and a software company
developer. No dull conversation in that house at Christmas!
Therefore Lynn Margulis, she of the endosymbiotic theory and the Gaia Hypothesis, proposed that we call the eukaryotic, protruding, microtubule structures by a different and common name – the undulipodia (undul = swinging or swaying, as in undulation, and podia = foot).

The undilopdia are the filamentous extracellular projections of eukaryotic cells, so they would include both cilia and flagella. So now we have an organelle you’ve never heard of before, but you still know what it is. I like the idea, because teaching about flagella is fairly littered with the times you have to say, “These are prokaryotic flagella we’re talking about, not eukaryotic flagella,” or vice versa. Lynn’s a smart cookie, but sometimes she goes a little far afield – we’ll see this as we talk more about undulipodia.

Next week, let’s look at the structure of undulipodia, compare them to prokaryotic flagella and wonder why rabbits get to be the exceptions.

Lahti, D. C., N. A. Johnson, et al. (2009). Relaxed selection in the wild. Trends in Ecology and Evolution, , 24 (9), 487-496

Stone G, & French V (2003). Evolution: have wings come, gone and come again? Current biology : CB, 13 (11) PMID: 12781152

Wiens JJ (2011). Re-evolution of lost mandibular teeth in frogs after more than 200 million years, and re-evaluating Dollo's law. Evolution; international journal of organic evolution, 65 (5), 1283-96 PMID: 21521189

For more information or classroom activities, see:

Undulipodia –

Convergent evolution –

Homologous structures –

Parallel  evolution –