Thy fearful symmetry

Everyone knows that most living things are symmetrical, and the vast majority of them bilaterally symmetrical (i.e. a single line down the midsection divides the organism into two mirror-image pieces).  A few are radial -- where any line through the center point divides it in half -- such as jellyfish and sea anemones.  Even symmetrical organisms like ourselves aren't perfectly so; our hearts and spleens are displaced from the midline toward the left, the appendix to the right, and so forth.  But by and large, we -- and the vast majority of living things -- have some kind of overall symmetry.

True asymmetry is so unusual that when you see it, it really stands out as weird.  Consider the bizarre-looking flounder:

[Image licensed under the Creative Commons Peter van der Sluijs, Large flounder caught in Holland on a white background, CC BY-SA 3.0]

Flounders start out their lives as ordinary little fish, upright with symmetrically-placed eyes, fins, and so on.  But as they mature, their skulls twist and flatten, and they end up with both eyes on the same side of the head -- a great adaptation for a fish that spends its life lying flat on the seabed, and who otherwise would constantly have one eye pointing downward into the mud.

A question I've asked here before has to do with the constraints on evolution; which of the features of life on Earth are so powerfully selected for that we might expect to see them in life on other planets?  (An example of one that I suspect is strongly constrained is the placement of the sensory organs and brain near the front end of the animal, pointing in the direction it's probably moving.)  But what about symmetry?  There's no obvious reason why bilateral symmetry would be constrained, and it seems as if it might just be a holdover from the fact that our earliest ancestors happened to be bilateral, so we (with a few stand-out exceptions) have inherited it down through the eons from them.

What about symmetry in general, however?  If we went to another life-bearing planet, would we find symmetrical organisms, even if they differ in the type of symmetry from ours?

The answer, judging from a paper that appeared this week in Proceedings of the National Academy of Sciences, by a team led by Iain Johnston of the University of Bergen, appears to be yes.

What Johnston and his team did was analyze the concept of symmetry from the perspective of information theory -- not looking at functional advantages of symmetry, but how much information it takes to encode it.  There are certainly some advantages -- one that comes to mind is symmetrically-placed eyes allows for depth perception and binocular vision -- but it's hard to imagine that's a powerful enough evolutionary driver to account for symmetry in general.  The Johnston et al. research, however, takes a different approach; what if the ubiquity of symmetry is caused by the fact that it's much easier to program into the genetics?

The authors write:

Engineers routinely design systems to be modular and symmetric in order to increase robustness to perturbations and to facilitate alterations at a later date.  Biological structures also frequently exhibit modularity and symmetry, but the origin of such trends is much less well understood.  It can be tempting to assume—by analogy to engineering design—that symmetry and modularity arise from natural selection.  However, evolution, unlike engineers, cannot plan ahead, and so these traits must also afford some immediate selective advantage which is hard to reconcile with the breadth of systems where symmetry is observed.  Here we introduce an alternative nonadaptive hypothesis based on an algorithmic picture of evolution.  It suggests that symmetric structures preferentially arise not just due to natural selection but also because they require less specific information to encode and are therefore much more likely to appear as phenotypic variation through random mutations.  Arguments from algorithmic information theory can formalize this intuition, leading to the prediction that many genotype–phenotype maps are exponentially biased toward phenotypes with low descriptional complexity.

Which is a fascinating idea.  It's also one with some analogous features in other realms of physiology.  Why, for example, do men have nipples?  They're completely non-functional other than as chest adornments.  If you buy intelligent design, it's hard to see what an intelligent designer was thinking here.  But it makes perfect sense from the standpoint of coding simplicity.  It's far easier to have a genetic code that takes the same embryonic tissue, regardless of gender, and modifies it in one direction (toward functional breasts and nipples) in females and another (toward non-functional nipples) in males.  It would take a great deal more information-containing code to have a completely separate set of instructions for males and females.  (The same is true for the reproductive organs -- males and females start out with identical tissue, which under the influence of hormones diverges as development proceeds, resulting in pairs of very different organs that came from the same original tissue -- clitoris and penis, ovaries and testicles, labia and scrotum, and so on.)

So symmetry in general seems to have a significant enough advantage that we'd be likely to find it on other worlds.  Now, whether our own bilateral symmetry has some advantage of its own isn't clear; if we landed on the planets orbiting Proxima Centauri, would we find human-ish creatures like the aliens on Star Trek, who all looked like people wearing rubber masks (because they were)?  Or is it possible that we'd find something like H. P. Lovecraft's "Elder Things," which had five-way symmetry?

And note that even though the rest of its body has five-way symmetry, the artist drew it with bilateral wings. We're so used to bilateral symmetry that it's hard to imagine an animal with a different sort. [Image licensed under the Creative Commons Українська: Представник_Старців (фанатський малюнок)]

So that's our fascinating bit of research for today; coding simplicity as an evolutionary driver.  It's a compelling idea, isn't it?  Perhaps life out there in the universe is way more similar to living things down here on Earth than we might have thought.  Think of that next time you're looking up at the stars -- maybe someone not so very different from you is looking back in this direction and thinking, "I wonder who might live on the planets orbiting that little star."

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The battle of the sexes

Today I'm going to tell you about the latest weird and fascinating research in genetics, but first, a brief refresher from high school biology to set the context.

You may recall that back in the 1800s, an Austrian monk named Gregor Mendel made the first serious stab at trying to figure out how inheritance works.  Prior to this, about all they knew was "like begets like," which sometimes works and sometimes leads you to think that there's such thing as "royal blood," despite evidence to the contrary such as the fact that a lot of those royals were nuttier than squirrel shit.

Anyhow, Mendel studied some traits in pea plants that seemed to obey a few statistical rules.  He made the understandable error of concluding that all traits inherit according to those rules, which turned out to be wrong; actually "Mendelian" traits, that obey all four of Mendel's Laws, are in the minority.  But for a first-order approximation, it wasn't bad. 

One trait in humans that is Mendelian is the Rh blood group gene.  Some people have a gene that makes the Rh protein; in others, the gene is defective, and makes nothing.  You only need one copy of the Rh-producing gene to have the Rh protein in your blood ("Rh-positive"), so the Rh-producing gene is said to be dominant; you only lack the protein ("Rh negative") if both of your copies of the gene are defective, so the non-functional gene is said to be recessive.

Since everyone has two copies of every gene -- one came from your mother, the other from your father -- this makes the inheritance pattern for Rh pretty simple.  (The "everyone has two copies" rule is broken by sex-linked genes, but this doesn't affect today's topic and is a subject for another day.)  Let's say, for example, that parent 1 is Rh-negative (so both copies are defective), and parent 2 is Rh-positive but has one defective and one normal copy.  Their kids inherit a defective copy from parent 1 (that's all (s)he's got), and the one that inherits from parent 2 has a 50/50 probability of being the normal or the defective one.  So the kids each have a 50% chance of being negative or positive.

The important part here is that I didn't stipulate which parent was which; in fact, it doesn't matter.  It works exactly the same way if the mom is parent 1 as it does if the dad is parent 1.

Okay, here's the second bit of background.  There's a group of terrible genetic defects called deletions, in which one of the patient's chromosomes broke somewhere along the process, and is missing a big chunk of genetic information.  You're supposed to have 23 matched pairs, one of each pair from dad and one from mom (again, ignoring the sex chromosomes).  In a deletion, when you match them up (a process called karyotyping) you find that one of the pairs isn't matched, because one member of the pair has a piece missing.

A karyotype for an individual with a deletion on the long arm of chromosome 4 (indicated by the arrow)

Each chromosome contains genes that guide development, and a person with a deletion only has a single copy of the genes in the deleted segment rather than the usual two.  The result is that (s)he only produces half the normal amount of the product made by that gene, and fetal development goes seriously awry.  Most deletions are so bad that they result in death of the embryo and miscarriage; the ones who survive to birth usually have drastic physical and mental abnormalities.

Once again, in the description of deletion, there's no indication which parent the broken chromosome came from.  In the above karyotype, you can't tell if the abnormal copy of chromosome 4 came from the mom or from the dad.  Shouldn't matter, right?  Mendel showed that the trait expresses the same way regardless which parent contributed what to the offspring.

With me so far?  Because here's where it gets a little weird.

The first inkling we had that there was more to the story came from a pair of genetic disorders that seemed, on first glance, to have absolutely nothing in common.  Angelman syndrome results in severe physical and developmental problems, including jerky or spastic movement of the limbs, little capacity for speech, cognitive impairment, and difficulty gaining and keeping on weight.  They often have no interest in food, so their diet has to be carefully managed.  Prader-Willi syndrome causes abnormal skull and brain growth, weak muscles, small hands and feet, and -- most strikingly -- an insatiable fixation on eating.  A friend of mine who worked in a home for the developmentally disabled once told me about a teenager who lived there who suffered from Prader-Willi syndrome, and he was so unable to control his hunger that he'd raid people's desks for food, and if that didn't work, he'd eat inedible things like chalk.

So nothing alike, are they?  Imagine researchers' puzzlement when they found out that both disorders were caused by the same deletion -- the loss of a chunk of the long arm of chromosome 15.

How could the same genetic damage result in such differing outcomes?  You're probably already guessing, given what I said earlier, that it has to do with which parent the damaged chromosome came from, and if so, you're right.  If the deletion was on the maternal copy of the chromosome, the child gets Prader-Willi syndrome; if it's the paternal copy, (s)he gets Angelman syndrome.

This was the first example ever discovered of the phenomenon of genomic imprinting -- where the gene expresses differently depending which parent it comes from.  But there's an even more curious part of the Prader-Willi/Angelman situation, and it has to do with hunger.

Let's say you're a male proto-hominid on the African savanna, and your significant other has just told you that you're gonna be a proud proto-hominid father.  The fetus is surviving inside the mom by obtaining nutrients through the placenta, so in essence, the baby is existing as a parasite on the mom (which continues even after birth, because of breastfeeding).  The dad's interest is (in the pure evolutionary sense) having the baby feed as much as possible, even at the expense of the mother; after all, the baby is his genes' way of surviving, and if the mom weakens, he can always find another mate.  The mom, on the other hand, certainly wants the baby to survive (half the baby's genes come from her, after all), but for her to survive is actually more important.  It's the opposite of the dad's situation; if the baby dies, she can have another baby, but if she dies, she's done for.

So the dad's imprint on the genes is to have the baby feed insatiably; the mom's imprint is to limit the baby's feeding to a level that isn't deleterious to her.  The system all works fine as long as the baby inherits copies of the imprinted genes from both parents; the competing interests of the mother and father balance each other out.  

But in a chromosome 15 deletion, that balance doesn't happen.  A baby with Angelman syndrome only has the maternal copy of a gene called UBE3A, and during egg formation, this gene is imprinted, with the result that it pushes the baby toward the mother's end of the spectrum, feeding-wise.  Thus the lack of interest in food you seen in kids with Angelman syndrome.  In Prader-Willi syndrome, the baby only has the paternal copy -- so the father's interest wins, and the kid wants to eat continuously.

All of this is lead-up to the research that came out last week in the journal Developmental Cell, in which a team of geneticists at Cambridge University found out that the missing chunk of chromosome 15 doesn't just cause opposite behavioral disorders depending on which parent it comes from; it actually changes the number of blood vessels that develop in the placenta long before the baby is born.  A gene called IGF2 (also in the target region of chromosome 15) controls the rate of blood vessel growth, and once again, it's in the dad's interest to have as many blood vessels as possible (favoring the baby at the expense of the mother) and in the mom's interest to inhibit blood vessel growth (favoring the mother at the expense of the baby).  And once again, if both copies are present and work correctly, the competing interests balance out, and the placenta develops normally -- resulting in an at-term overall length of blood vessels of 320 kilometers if you stretched them out end to end.  The genomic imprinting shows up, though, if one of the copies of the genes is defective or missing, because then the parent that contributed the working copy "wins."

So that's another odd twist on inheritance and development, for your morning entertainment.  It all brings to mind the comment made by my genetics professor, Dr. Lemmon, when I was an undergraduate.  "It's not strange when something goes wrong with our developmental genetics," she told us.  "There are a million ways things could go wrong.  What's phenomenal is how often everything goes right."

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Neil deGrasse Tyson has become deservedly famous for his efforts to bring the latest findings of astronomers and astrophysicists to laypeople.  Not only has he given hundreds of public talks on everything from the Big Bang to UFOs, a couple of years ago he launched (and hosted) an updated reboot of Carl Sagan's wildly successful 1980 series Cosmos.

He has also communicated his vision through his writing, and this week's Skeptophilia book-of-the-week is his 2019 Letters From an Astrophysicist.  A public figure like Tyson gets inundated with correspondence, and Tyson's drive to teach and inspire has impelled him to answer many of them personally (however arduous it may seem to those of us who struggle to keep up with a dozen emails!).  In Letters, he has selected 101 of his most intriguing pieces of correspondence, along with his answers to each -- in the process creating a book that is a testimony to his intelligence, his sense of humor, his passion as a scientist, and his commitment to inquiry.

[Note: if you purchase this book using the image/link below, part of the proceeds goes to support Skeptophilia!]

Changing the thermostat

Everyone knows that the human core body temperature is supposed to be around 98.6 F.  At least, that's what we all learned in seventh grade life science, right?

A more curious question is why 98.6 and not some other temperature.  Other mammals need different core body temperatures, but the range is remarkably narrow -- from elephants (97.7 F) to goats (103.4 F), only a 5.7 degree difference overall, and the vast majority of mammal species are in the vicinity of 98-100 F.

In my biology classes, I usually did nothing more than a hand-waving explanation that "our body temperatures are what they are because that's the temperature where our enzymatic and neurochemical reactions work at their optimal rate," but that's a facile analysis at best -- a bit like saying "bake the cake at 350 F because 350 F is the best temperature at which to bake cakes."  It might be true, but it doesn't tell you anything.

Last month we got a better explanation of what's going on than what I used to give (admittedly a low bar).  A paper in Molecular Cell with the daunting title, "A Conserved Kinase-Based Body-Temperature Sensor Globally Controls Alternative Splicing and Gene Expression," by a huge team led by Tom Haltenhof of Freie Universität Berlin's Department of Biochemistry, gives us a window into why we regulate body temperature -- and why things fall apart so quickly when the temperature isn't what it should be.

The team looked at the effects of temperature change not in mammals but in turtles and crocodiles -- which are themselves poikilothermic (known in common parlance as "cold-blooded") but have a temperature-switching mechanism for sex determination.  In crocodiles, incubation of the eggs at a warmer temperature results in males; in turtles, the pattern is the opposite.  (Some lizards have an even odder pattern, where intermediate temperatures result in males, and either low or high temperatures result in females.)

The question was how this was happening.  Something about the temperature must be changing the chemical signaling that guides embryonic development; but how?

Haltenhof's team found that there is a group of enzymes called CDC-like kinases that are extremely temperature-sensitive.  Kinases in general are a hugely important enzyme family that are responsible for phosphorylation, the main way energy is transferred in living organisms.  So if you affect the reaction rate of a kinase, it results in changes in the transfer of energy -- and can have enormous impacts on the organism.

And the CDC-like kinases, Haltenhof et al. found, were acting directly on the DNA, and changing the rate of gene expression.  In crocodiles and turtles, the type of gene expression affected had to do, unsurprisingly, with embryonic development of the reproductive systems.

So far, interesting only to geneticists and herpetologists (and, presumably, to the crocodiles and turtles themselves).  But where it caught my attention was when it was pointed out that the activity of CDC-like kinases is important not only in reptiles, but in humans -- and that overexpression of one of them, cyclin E, is connected with at least one form of cancer.

So this research seems to have implications not only for embryonic development in crocodiles and turtles, but in explaining why our own body temperatures are so tightly regulated.  The authors write: "[CDC-like kinase] activity is likely to also impact on gene expression in pathological conditions such as hypothermia, septic shock, and fever, or in the slightly warmer tumor microenvironment."  And since in general, the core body temperature drops as a person ages, it also made the authors speculate that this could be the key to at least some age-related malfunctions (and perhaps suggest a way to treat them).

[Image licensed under the Creative Commons 24ngagnon, Thermostat science photo, CC BY-SA 4.0]

This also brought to mind another perplexing bit of research that came out in January -- that the average human body temperature is dropping, on the order of 0.03 C per decade.  The standard "98.6 F" was established in 1851 by Carl Reinhold August Wunderlich, who determined this by taking the axillary (armpit) temperature of 25,000 people in Leipzig (and you thought your job was boring).  But a recent study with even more measurements found that currently, the average body temperature is almost a degree cooler than Wunderlich's value.

The speculation in that paper is that the drop in temperature is due to a decrease in the inflammation caused by exposure to infectious agents.  If the 25,000 Leipzig residents were a representative sample from the mid-19th century, 3% would have had an active tuberculosis infection, and that's just one disease.  So the lower average temperature today might have to do with our lower incidence of infections of various kinds.

But it makes me wonder what effect that's having on the CDC-like kinases from the first study.  Because during our evolutionary history, the 1850s condition of harboring infections was much more the norm than our current clean, germ-free-ness.  So while losing our collection of nasty bacteria might be overall a good thing, it might have caused a drop in temperature that could affect other reactions -- ones we're only beginning to understand.

That's yet to be established, of course.  But what it does highlight is how important the body's thermostat is.  Only a four-degree drop in core body temperature is a sufficient level of hypothermia to severely endanger a person's survival; likewise, a six-degree increase would be a life-threatening fever that (if survived) could result in brain damage.  We are only beginning to understand how our temperature is regulated, and why the effects of losing that regulation are so drastic.  But what this new research shows is that our body temperature might have far more ramifications for our health than we ever imagined -- and could be the key to understanding, and perhaps treating, diseases that have up till now defied medical science.

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This week's Skeptophilia book-of-the-week is brand new -- science journalist Lydia Denworth's brilliant and insightful book Friendship: The Evolution, Biology, and Extraordinary Power of Life's Fundamental Bond.

Denworth looks at the evolutionary basis of our ability to form bonds of friendship -- comparing our capacity to that of other social primates, such as a group of monkeys in a sanctuary in Puerto Rico and a tribe of baboons in Kenya.  Our need for social bonds other than those of mating and pair-bonding is deep in our brains and in our genes, and the evidence is compelling that the strongest correlate to depression is social isolation.

Friendship examines social bonding not only from the standpoint of observational psychology, but from the perspective of neuroscience.  We have neurochemical systems in place -- mediated predominantly by oxytocin, dopamine, and endorphin -- that are specifically devoted to strengthening those bonds.

Denworth's book is both scientifically fascinating and also reassuringly optimistic -- stressing to the reader that we're built to be cooperative.  Something that we could all do with a reminder of during these fractious times.

[Note: if you purchase this book using the image/link below, part of the proceeds goes to support Skeptophilia!]

Clone war

The idea of human clones has been a staple of science fiction for decades.  Whenever the topic comes up, the question is always whether it's even theoretically possible to clone a person.

The answer seems to be "yes, but."  Embryonic cloning -- splitting a blastula (an early stage of embryonic development) into pieces, and allowing the pieces to regrow into a full embryo -- is relatively straightforward.  There's no scientific reason that someone couldn't take a human blastula, cut it into twenty pieces, and when they've regrown sufficiently implant them in the uteruses of twenty different surrogate women -- and nine months later, if all goes well, you'd have identical twenty-tuplets, all born to different women.

Much trickier is adult-tissue cloning, which is the more common one to see in science fiction; taking a sample of tissue from an adult, and somehow transforming it into a zygote, and ultimately, an embryo. The reasons why this is hard are not fully understood, but seem to have something to do with the switching on and off of developmental genes, something that has to happen with great precision in order to generate a fully functional, anatomically normal child.  So to make this work, you have to be able to reset all those switches back to their (so to speak) factory specifications -- return them to where they were when the embryo was still an undifferentiated ball of cells.

For reasons still not known, this appears to be more easily doable in some organisms than others.  The first adult-tissue clone was the famous Dolly the Sheep, who was born back in 1996.  Dolly died at age six -- about half the age of a normal sheep -- which scientists initially thought was because of accelerated aging (that her cells retained a "memory" of the age of the sheep from which they were taken).  Later experiments called this into question, and the jury's still out on whether clones would age faster, and presumably, die younger.

[Image licensed under the Creative Commons (Photograph courtesy of Emma Whitelaw, University of Sydney, Australia.), Cloned mice with different DNA methylation, CC BY 2.5]

So far, the list of animals that have been adult-tissue cloned is a curious one.  You can take a look at the complete list as of the time of this writing, but it includes a bunch of not-very-closely-related species -- frogs, rabbits, rats, monkeys (two species, in fact), mules, coyotes, both cats and dogs, and camels.

Note that humans aren't on the list.

Which makes it doubly odd that a rapper who goes by the moniker "Lil Buu" claims not only to be a clone, but a "second-generation clone," whatever that means.  On a television interview, Lil Buu said:

I was cloned by clonaid in Canada, my model number is 0112568…  A lot of the memories from Clonaid were erased so that way the new gen can move forward with whatever new programming was made….  They can remove a fragment of bone that’s located here [points to forehead, in between his eyes], and in this fragment of bone it stores all of your memories and consciousness, and with that, they can make a sufficient replica of yourself, a reproductive version of you including your memories, and you can be selective as to which ones you keep and don’t keep.  This process has been around for quite some time.

Immediately I read about Clonaid, that made my eyebrows rise even further.   I don't know if that name is familiar to you, but it certainly was to me; this is the group that back in 2002 claimed they'd overseen the production of the first human clone (a girl nicknamed "Eve"), but then refused to provide scientists with any proof, or in fact any evidence at all.  Then it turned out that the spokesperson for Clonaid who was said to be the chief scientist in charge of the project, Brigitte Boisselier, is a high-ranking Raëlian -- a French-based religion, founded by ex-race-car-driver turned prophet Claude Maurice Marcel Vorilhon, that believes humans were created by a race of extraterrestrials called Elohim, and to gain enlightenment we need to run around having lots of sex with any willing individuals, and wear no clothes whenever possible.

I'm not making any of this up.

Oh, and they have a temple in Japan called "Korindo," are working on establishing an "Embassy for Extraterrestrials," and their symbol is a swastika superimposed on a Star of David.

For the record, I didn't make that up, either.

So I'm perhaps to be forgiven for being dubious about Lil Buu (or model #0112568, as the case may be) and his claim to be a cloned from a memory-containing bone fragment, who was produced by a company whose leaders believe we're actually the creation of super-intelligent aliens, which was dreamed up by a guy whose primary other claim to fame is knowing a lot about race cars.

In fact, I'm dubious in general about the potential for human cloning.  It raises some serious ethical issues, and (after all) we haven't even resolved the ethical issues surrounding stem cell research and cloning non-human animals, so it's premature to leap headlong into this.

It also brings up the question about why anyone would want to clone themselves.  It's not like the clone would have your memories (whatever Lil Buu says to the contrary); our personalities are shaped not only by our genes but by our environment, so while you'd expect some similarities, they would be no more alike than ordinary identical twins -- who are, after all, natural clones themselves.

Plus, I just think it'd be creepy for there to be another me walking around, one who would be (if he was created as an embryo today) 59 years younger than I am by the time he's born.  I'm perfectly happy being a one-off.  My general feeling is that one of me is plenty.

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I've been a bit of a geology buff since I was a kid.  My dad was a skilled lapidary artist, and made beautiful jewelry from agates, jaspers, and turquoise, so every summer he and I would go on a two-week trip to southern Arizona to find cool rocks.  It was truly the high point of my year, and ever since I have always given rock outcroppings and road cuts more than just the typical passing glance.

So I absolutely loved John McPhee's four-part look at the geology of the United States -- Basin and Range, Rising From the Plains, In Suspect Terrain, and Assembling California.  Told in his signature lucid style, McPhee doesn't just geek out over the science, but gets to know the people involved -- the scientists, the researchers, the miners, the oil-well drillers -- who are vitally interested in how North America was put together.  In the process, you're taken on a cross-country trip to learn about what's underneath the surface of our country.  And if, like me, you're curious about rocks, it will keep you reading until the last page.

Note: the link below is to the first in the series, Basin and Range.  If you want to purchase it, click on the link, and part of the proceeds will go to support Skeptophilia.  And if you like it, you'll no doubt easily find the others!

Mechanical brain transplant

New from the "Well, I can't see any way that could go wrong, do you?" department, we have: scientists growing Neanderthal brain fragments in petri dishes and then connecting them to crab-like robots.

My first thought was, "Haven't you people ever watched a science fiction movie?"  This feeling may have been enhanced by the fact that just a couple of days ago I watched the Dr. Who episode "The End of the World," wherein the Doctor and his companion are damn near killed (along with everyone else on a space station) when a saboteur makes the shields malfunction using little scuttling metallic bugs.

The creator of the Neanderthal brain bits is Alysson Muotri, geneticist at the University of California - San Diego's School of Medicine.  He and his team isolated genes that belonged to our closest cousins, Homo sapiens neanderthalensis, and transferred them into stem cells.  Then, they allowed the cells to grow into proto-brains to see what sorts of connections would form.

Muotri says, "We're trying to recreate Neanderthal minds."  So far, they've noticed an abnormally low number of synapses (as compared to modern humans), and have speculated that this may indicate a lower capacity for sophisticated social behavior.

But Muotri and his team are going one step further.  They are taking proto-brains (he calls them "organoids") with no Neanderthal genes, and wiring them and his "neanderthalized" versions into robots, to make comparisons about how they learn.  Simon Fisher, a geneticist for the Department of Psycholinguistics at the Max Planck Institute, said, "It's kind of wild.  It's creative science."

That it is.

I have to admit there's a cool aspect to this.  I've always wondered about the Neanderthals.  During the peak of their population, they actually had a brain capacity larger than modern humans.  They clearly had culture -- they ceremonially buried their dead, probably had language (as they had the same variant of the "linguistic gene" FOXP2 that we do), and may have even made music, to judge by what appears to be a piece of a 43,000 bone flute that was found in Slovenia.

All that said, I'm not sure how smart it would be to stick a Neanderthal brain inside a metallic crab.  If this was a science fiction movie, the next thing that happened would be that Muotri would be in his lab late at night working with his Crab Cavemen, and he'd turn his back and they'd swarm him, and the next morning all that would be found is his skeleton, minus his femur, which would have been turned into a clarinet.

Okay, I know I'm probably overreacting here.  But it must be admitted that our track record of thinking through our decisions is not exactly unblemished.  Muotri assures us that these little "organoids" have no blood supply and therefore no potential for developing into an actual brain, but still.  I hope he knows what he's doing.  As for me, I'm going to go watch Dr. Who.

Let's see, what's the next episode?  "Dalek."  *reads description*  "A superpowerful mutant intelligence controlling a mechanical killing device goes on a rampage and attempts to destroy humanity."

Um, never mind.  *switches channel to Looney Tunes*

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This week's book recommendation is from one of my favorite writers and documentary producers, Irish science historian James Burke.  Burke became famous for his series Connections, in which he explored the one-thing-leads-to-another phenomenon which led to so many pivotal discoveries -- if you've seen any of the episodes of Connections, you'll know what I mean when I say that it is just tremendous fun to watch how this man's brain works.  In his book The Pinball Effect, Burke investigates the role of serendipity -- resulting in another tremendously entertaining and illuminating read.