Wednesday, October 22, 2014

Death By Haunted House


Halloween is a time when fear is invited. The rush of
adrenaline in a controlled environment is life-
affirming. Not much else to comment on here,
except that he seems to have excellent oral hygiene
for a chainsaw-wielding maniac.
A big man with the chainsaw and the gaping wound on his face jumps out from around the corner and growls. You leap backward and scream, your heart pounding in your ears. You’re ready to either take that power tool and teach him a lesson or to run like the kid from Home Alone. Sure you're scared, but could it kill you?

Haunted houses are great examples of stimuli that induce the fight or flight response. The name suggests that two mechanisms are fighting it out, but there is really only one biologic pathway. Whether an animal tries to escape or tries to defend itself, its muscles and mind need to be ready.

In response to a threat, the brain triggers the release of epinephrine and cortisol from your adrenal glands into the blood. As a result, your heart beats faster and stronger, your blood vessels dilate to move more blood, and your lung vessels dilate to exchange more oxygen for carbon dioxide. Equally as important, your liver breaks down glycogen (a sugar storage molecule) to glucose and dumps it into your bloodstream.

All these processes work together to increase your alertness and increase the power of your muscles for a short time - like when mothers who lift cars off their small children. You are now ready to respond to the threat; however, there is an exception – you may do nothing at all.

One of the major control mechanisms of the fight or flight response is the autonomic nervous system. This is part of the peripheral nervous system (PNS, outside the brain and spinal cord) and transmits information from the central nervous system to the rest of the body. The autonomic system controls involuntary movements and some of the functions of organs and organ systems.

Parts of the autonomic system acts like a teeter-totter, it's their relative balance that controls the outcomes. In the fight or flight response, the sympathetic system predominates and your heart rate increases and your blood vessels dilate.

The autonomic nervous system is divided into sympathetic
and parasympathetic. Much of the sympathetic innervation
comes from the thoracic and lumbar regions, while most
parasympathetic innervation is carried by the vagus nerve.
You can see that the two systems have largely opposite effects.
But what if the parasympathetic system gained an upper hand for a short time? The parasympathetic system controls what is sometimes called the rest and digest response – the opposite, get it? The heart slows, the blood vessels constrict in the muscles, blood moves from muscles to the gut, and glycogen is produced from glucose. Remember the old adage - don’t swim after your dine; eating puts you in a parasympathetic state of mind! (O.K., I just made it up)

Many people have had the experience of parasympathetic domination coincident to a threat, for some folks it proceeds long enough to have an observable result – they faint. The vagus nerve (a primarily parasympathetic cranial nerve) controls much of this response, so it may be called the vasovagal response. The parasympathetic-mediated reduction in blood oxygen and glucose do not spare the brain - and when your brain is starved of oxygen and glucose, you pass out. Fighting or fleeing is difficult when you are unconscious.

Lower animals will faint as well, but they have additional defenses along these lines. Mammals, amphibians, insects and even fish can be scared enough to fake death – ever hears of playin’ opossum?

There are overlapping mechanisms for feigned death, from tonic immobility (not moving) to thanatosis (thanat = death, and osis = condition of, playing dead). When opossums employ thanatosis, they fall down, stick their tongue out, and even emit a foul smelling odor from glands around their anus. One study in crickets showed that those who feigned death the longest were more likely to avoid being attacked, so this is definitely a survival adaptation – except for the opossums scared by cars and decide to play dead in the street.

Feigned death deters predation, so being scared ain’t all bad. Many predators won’t eat something that is already dead, so not moving could protect them from attack. Another theory is the clot formation hypothesis; it contends that slowing the heart and blood flow forces blood clots to form faster. This will reduce the amount of blood lost during an attack, improving chances for survival.

New evidence is suggesting that even humans undergo tonic immobility. Post-traumatic stress patients asked to relive their trauma show definite signs of tonic immobility, although first they show signs of "attentive immobility," which is more voluntary then the tonic form.

I highly recommend this new book for popular
biology and medicine readers. Zoobiquity explores
a powerful reality. No disease--whether physical or
psychiatric--is uniquely  human. We have much to
learn from animal patients and from the doctors who
care for them.  The impact on human medicine
will be significant.
We have discovered one exception to the rule; instead of fight or flight, it is really fight, flight or faint – but can we take it further? Should it be fight, flight, faint, or fatality? The answer is yes, but it's very rare. Sometimes animals (including us) don’t just feign death when afraid – they actually die.

In their book, Zoobiquity, What animals can teach us about health and the science of healing, Barabara Natterson-Horowitz and Kathyrn Bowers talk about capture myopathy in animals. Small traps that limit movement, cause pain, or are associated with loud noises can cause spontaneous death in live-trapped animals. Several decades ago it was not unusual for 10% of trapped animals to die. In birds, the death rate often rose to 50%! More humane methods of live trapping have reduced the death rate, but point is made – these animals were scared to death.

A human analogy of capture myopathy may have been identified. People that have had a sudden emotional shock, perhaps the death of a loved one, some other tragic occurrence, or crippling fear can undergo something that looks a lot like a heart attack, even if they have no history of heart disease.

This sudden loss of heart rhythm has been called broken-heart syndrome, but is more accurately termed stress cardiomyopathy (SCM). In these cases, the heart actually changes shape! The part of the heart that pumps blood out to the body (left ventricle) balloons out and loses the ability to pump efficiently. Dramatically less efficient pumping leads to symptoms just like a heart attack.

In the normal left ventricle of the heart (left image), the muscle is
thick around the space (in red) and contracts strongly. In SCM, the
space is ballooned at the based (middle image) and the muscular wall
is thin, giving a weak contraction. The change in shape can be seen in
the superimposed images on the right, as is the octopus trap (tako-tsubo)
that the original Japanese describers thought the lesion looked like,
hence the early name takotsubo cardiomyopathy.
In most cases, SCM and the change in heart shape resolve after a time and there is little left to show they were present, but if they go too far for too long, they can cause death – called sudden cardiac death. There are many causes for sudden cardiac death, but emotion and fear are definitely among them.

I was wondering if there was a link between SCM in humans and capture myopathy in animals, so I asked Dr. Natterson-Horowitz. She told me that those studies have not been done yet; we don’t know if there is a heart shape change in captured animals. I think it would be hard to get approval for studies that would intentionally scare animals to death.

One interesting connection amongst fight or flight, capture myopathy, and SCM is the catecholamine dump involved. Epinephrine and norepinephrine control all three responses, and in humans they control even more. Recent evidence shows that catecholamines mediate the production of fear memories.

You remember fearful events more readily and more vividly as a survival adaptation. Strong memories help you to avoid dangerous situations in the future. In this way, your mind can affect how your body responds to a threat. We will see this again in just a bit.

All babies have an exaggerated startle reflex until
they are several months old, but in some cases it may
contribute to SIDS. An exaggerated startle can lead to
apnea (temporary breathing cessation) and this can be
compounded by a depressed heart rate if the baby is
sleeping on its stomach. Some clinicians also theorize
that swaddling may contribute by exaggerating the startle
due to confinement stress, but by far the greatest
association with SIDS is stomach sleeping.
However, dying or nearly dying from fright isn’t all in your head either; some conditions can predispose you to dying from a sudden shock. One unfortunate condition is called hyperekplexia, or startle disease of the newborn. Newborns with one or more of several mutations in the glycine receptor (an inhibitory receptor in the brain used in neuron signal transmission) can lead to these babies dying from loud noises or a sudden touch.

The startle reflex involves squinting to protect the eyes, raising the arms, hunching the body to protect the back of the neck, as well as inducing the fight or flight response. With the loss of inhibitory signaling, the signals that ramp up a startle response are unchecked and can lead to uncontrolled beating of the heart (ventricular fibrillation, VF) and sudden cardiac death.

Just as some cases of the fight or flight response going too far, the startle can sometimes lead to VF. A recent study has shown that the bigger the perceived threat, the bigger the startle reflex will be. Also, if there is a fearful environment prior to the threat, then the startle will be bigger. Once in a long while, it goes too far.

Similar to hyperekplexia, there is another condition that could lead to VF and death in the environment of fear. Long QT syndrome can either be inherited or acquired later in life, and affects the time between beats of the heart. In long QT, the interval is variable and longer, and can lead to inefficient beating and VF.

On echocardiogram tracings a heartbeat has a certain shape, and 
each point has a corresponding name which is represented 
by a letter. If the time between the Q point and the T point 
is too long, the heart rhythm is subject to disintegrating 
into chaos. In the 1990’s, the antihistamine Seldane was 
taken off the market due to QT interaction when it was 
given with the antibiotic erythromycin.
Highlighting our circle of fear and the body, evidence presented here and here suggest that SCM can cause acquired long QT syndrome. Dr. Natterson-Horowitz said today many patients with long QT may have implantable defibrillators. In earlier days, however, these patients were warned not to use alarm clocks or to jump into cold water – they could startle themselves to death.

Long ago we talked about premature burial. It would be easy to envision a person waking up inside a coffin, and then dying from the fright of being buried alive! Does this mean that you are putting yourself in peril every time you visit a haunted house at Halloween? Probably not, remember that deaths from fright are exceedingly rare. Maybe you could just feign death, and the horrible monster will leave you alone.

For the next couple weeks - back to the science of flagella. Undulipodia are present in many phylums, except for where they aren’t. On the other hand, some types of organisms don’t have undulipodia - except for those that do.


Greek, R. (2012). Zoobiquity: What Animals Can Teach Us About Health and the Science of Healing. By Barbara Natterson-Horowitz and Kathryn Bowers. Knopf Doubleday Publishing: New York, NY, USA, 2012; Hardback, 320 pp; $16.23; ISBN-10: 0307593487 Animals, 2 (4), 559-563 DOI: 10.3390/ani2040559

Volchan, E., Souza, G., Franklin, C., Norte, C., Rocha-Rego, V., Oliveira, J., David, I., Mendlowicz, M., Coutinho, E., Fiszman, A., Berger, W., Marques-Portella, C., & Figueira, I. (2011). Is there tonic immobility in humans? Biological evidence from victims of traumatic stress Biological Psychology, 88 (1), 13-19 DOI: 10.1016/j.biopsycho.2011.06.002


For more information or classroom activities, see:

Fight or flight –

Autonomic nervous system –

Thantosis/tonic immobility –

Stress cardiomyopathy –

Hyperekplexia –

Long QT syndrome -


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 –