Martin Schaefer, one of the scientists I wrote about in my recent post on autumn leaves, has joined the comment thread and kindly answered some questions about his work. Check it out.

Flowers, flagella, feathers. Life is rife with complex features–structures and systems made up of many interacting parts. National Geographic magazine asked me to take a tour of complexity in life and report on the latest research on how it evolved. What struck me over and over again was how scientists studying everything from bacteria to humans are drawn back to the same concepts–making new copies of old parts, for example, or borrowing parts of one complex trait to evolve a new one. And in each case, complexity opens up the way to diversity, because something many parts can be rearranged in many ways. There’s not yet a general theory for the evolution of complexity, but scientists are certainly converging on some of the same themes.

My story, “A Fin Is A Limb Is A Wing,” is in the November 2006 issue of the magazine. When the new issue was posted to the National Geographic web site today, I was pleased to find that my article is not hidden away behind a subscription wall. You can read the whole thing here. The web site also has a gallery of Rosamund Purcell’s lovely (but slightly eerie) photographs that accompany the story.

I was intrigued to see that the magazine has a forum for each article. I tried to see what sort of comments had been posted about my story, but couldn’t get through. If anyone figures it out, let me know! (I’m also curious if I get the Mooney treatment for my efforts.)

To supplement National Geographic’s on-line features, I thought I’d point curious readers to a particularly good paper or scientific review for each of the examples I hit in the article. Behind my writing and Rosamund’s pictures is a massive wall of scientific research.

1. Multicellularity. “The unicellular ancestry of animal development.” Developmental Cell 2004.

2. Arthropod body segments. “Comparative developmental genetics and the evolution of arthropod body plans.” Annual Reviews in Genetics, 2005

3. Vertebrate Head. “The new head hypothesis revisited” Journal of Experimental Zoology B 2005.

4. Eyes. “Casting a genetic light on the evolution of eyes” Science 2006.

5. Limbs. “The pectoral fin of Tiktaalik roseae and the origin of the tetrapod limb.” Nature 2006

6. Feathers. “Evolution of the morphological innovations of feathers.” Journal of Experimental Zoology B 2005.

7. Flowers. “Flower development and evolution: gene duplication, diversification and redeployment.” Current Opinions in Genetics and Development, 2005

8. Flagella. “From The Origin of Species to the origin of bacterial flagella” Nature Reviews Microbiology 2006 [pdf]

This fall we’ve had some rude visitors out by the front door. One morning a strangely foul smell wafted through the windows. When we looked outside for a dead animal, we found nothing. But we noticed some downright obscene growths foisting themselves out of the flower beds. Thus I got my first introduction to the stinkhorn.

Stinkhorns are pornographic mushrooms. They form large underground webs of threads, which feed on dead and dying plant matter. At scattered points in the stinkhorn network, white rubbery spheres grow. Inside each of them is a pre-formed stinkhorn, which can then spring forth. The stinkhorns that grew outside our front door are called Phallus impudicus–Latin for the impudent penis. The stinkhorn expands with hydraulics that resemble the sort found in the human male anatomy. Water surges into honeycombed spaces, expanding the shaft out of its jellied egg. Stinkhorns can grow six inches an hour, with enough force to break through asphalt.

The stinkhorn looks like its phallic namesake, down to the small hole at the tip. Out of that hole comes The slimy mass on top of the mushrooms releases a stinky smell, carried by molecules that mimic the odor of corpses. Slugs and flies and other insects come from all around, swarming across the stinkhorn and feeding on its slime. They swallow the stinkhorn’s spores as well, which they will later release with their own excrement.

This was all new to me. For enlightenment, I turned to some mycologists–scientists who study mushrooms and other fungi for a living. (One of them, Nicholas Money, is the author of several books on fungi that I’d recommend.) To me, stinkhorns are further proof that fungi are the weirdest, most mysterious bunch of species one could imagine. Compared to fungi, even the most bizarre animals are easy to grok: they are like us in the basics, searching for food to ingest. Plants may be profoundly different than we are, harnessing the energy from the sun rather than finding living matter to devour. Still there’s something comfortable and soothing in the sight of a sunflower or a blossoming dogwood.

Fungi, on the other hand, are fundamentally alien. They send up stinkhorns and puffballs and fairy rings. They join with algae to form scab-like lichens. They are truffles and bread mold, Shitake mushrooms and yeast infections. Some lurk in the Earth, spreading out over hundreds of acres. Others live inside insects, forcing them to climb to the tip of a blade of grass, so that they can shower their spores down on new victims. Instead of ingesting their food, fungi dump their digestive enzymes into their surroundings and suck up the ensuing goo. Their reproductive cycles are like labyrinths. And of the estimated 1.5 million species of fungi on Earth, scientists have identified only five percent.

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As the autumn leaves turn handsomely, I’ve been wondering, why do trees bother? It’s a question scientists have been asking for the past few years, and for the first time, they’ve carried out an experiment to find out.

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This morning it was announced that two American scientists won the Nobel Prize in Physiology and or Medicine, for their 1998 discovery of a hidden network of genes. It may seem odd that a network of genes could lurk undiscovered for so long. But the cell is very much a mysterious place. In the 1950s, scientists established the basic model for how genes work. A gene is made of DNA, the cell makes a single-stranded copy of a gene in a molecule called RNA, and it then uses the RNA as a template for building a protein. This so-called Central Dogma proved to be correct for many thousands of genes, but not all of them. In many cases, a gene’s RNA is not a mere messenger. It grabs onto other RNA molecules or proteins, and carries out some important chemistry of its own.

Different RNA molecules carry out different kinds of chemistry. Scientists are a long way from figuring out everything they do, but they now understand a few sorts pretty well. This year’s Nobel–awarded to Craig C. Mello, a Howard Hughes Medical Institute investigator at the University of Massachusetts Medical School, and Andrew Z. Fire at Stanford University School of Medicine–recognizes one part of the RNA network, called RNA interference. A class of small RNA molecules can grab onto ordinary RNA molecules and destroy them.

This may seem like a harmful thing for a molecule to do, but it is actually essential to the proper workings of the cell. A cell needs to keep its proteins in balance, and that balance changes with changing conditions. Using RNA interference, a cell can quickly reduce or increase the amount of a specific protein to the proper level.

Like all great discoveries, Mello and Fire’s discovery of RNA interference has sent other scientists in all sorts of unexpected directions of research. Some have turned RNA interference into a powerful tool for probing the function of genes. They engineer silencing RNA to shut down a particular gene. They then observe what happens to an animal or a cell when it can no longer make the gene’s protein. RNA interference may also become a new path for medicine, allowing doctors to target troublesome genes.

Scientists have also been wondering about the history of RNA interference. Mello and Fire first discovered it in worms, but that does not mean it’s a quirk of those particular animals. In fact, RNA interference is widespread in animals, as well as in plants, fungi, and many other groups of species. Having compared their RNA interference genes, scientists have concluded that those genes are an ancient but still-evolving system for fighting off parasites.

In some cases, these parasites are invading viruses. Some viruses (such as the tobacco mosaic virus shown here) carry genes made of RNA instead of DNA. Their hosts can defend themselves against the viral genes with RNA interference, grabbing incoming virus RNA and cutting it apart. We and many other species carry a lot of virus-like pieces of DNA in our own genomes, too. These mobile elements, as they’re sometimes called, make RNA copies of themselves which then get converted back into DNA and inserted into other places in our genome. Almost half of our DNA is made up of these mobile elements. To slow the spread of these genomic parasites, many species use RNA interference to destroy their RNA copies.

All well and good–except that parasites evolve as well. A cell can only use RNA interference to defend itself against a virus if it can recognize the virus’s genes. If a virus mutates so that its RNA becomes hard to recognize (but still carries out its original function), it will evade the cell’s defenses. Viruses are also able to block RNA interference. They produce molecules that interfere with the enzymes that help prepare silencing RNA that will attack the viruses.

Hosts that can overcome these counterstrategies will be favored in turn by natural selection. And so virus and host get trapped in a coevolutionary arms race. In March, scientists at the University of Edinburgh estimated the speed of this evolution by comparing genes involved in RNA interfence from different species of Drosophila fruit flies. They found that new variants of these genes have emerged in the different species–even in populations of the same species. These variants reveal that RNA interference genes are rapidly evolving in fruit flies. In fact, they are among the fastest evolving genes in the fruit fly genome.

Fruit flies and humans use many similar genes to assemble interfering RNA molecules. So do plants and yeast. Scientists can trace the ancestry of some of these genes to a common ancestor of all living eukaryotes–one of the three main branches of the tree of life. That single-celled ancestor may have lived a couple billion years ago. It had a simple RNA-based defense system, which later became more elaborate in different lineages. The genes not only changed their targets, but also increased their targets, as accidental mutations created extra copies of the RNA interference genes. Along the way, RNA interference also took on new functions–not just fighting viruses, but keeping tight control over the cell’s own functions.

Bacteria are victims of viruses as well, and they appear to use their own RNA-interference system to fight them. But this system doesn’t appear to share a common ancestry with the one we and other eukaryotes use. Instead, they evolved their own set of genes. It’s a case of convergent evolution–the bat and bird wings of the RNA world. RNA interference may have been especially important four billion years ago, in the earliest stages of life on Earth. Many scientists have argued that DNA did not yet exist. Only RNA-based life covered the planet–both as self-sustaining organisms and their RNA viruses. Without any elaborate immune system made up of specialized cells, the RNA hosts would have clearly benefited from RNA interference. And viruses may have evolved some extraordinary counterdefenses–perhaps even the first copies of DNA.

(See also Pure Pedantry and other Scienceblog posts for other takes on the announcement.)

PZ Myers did an excellent job yesterday of dismantling the latest from intelligent-design advocate Jonathan Wells. Wells wrote a piece on WorldNetDaily called “Why Darwinism is Doomed.” It is based some new research identifying an important gene involved in the human brain–which I blogged about last month. Wells claims that this discovery is a serious threat to evolution. Why? Because scientists have only just found the gene, because many genes are involved in building the human brain, and because finding a gene that’s different in humans than in other animals doesn’t actually reveal what caused that difference. Myers shows why all three arguments are wrong.

If you rely on Wells, you will come away with an impression of how scientists look for new genes that is precisely the opposite of reality. The authors of the new paper did not simply scan through the human genome in the hopes of finding something interesting. The genome is too big and mysterious for that approach. It’s like searching the Pacific for an island. If you just wander the ocean randomly, you may die before landfall.

What made this particular search especially challenging was that the gene in question does not make a protein. Protein-encoding DNA makes up only two percent of the genome, and non-coding DNA is a murky realm of virus-like stretches of DNA, broken genes, and some genes that actually serve an important function. It is very difficult to look at a single genome and pick out functionally important segments of DNA from the “junk.”

So how did the scientists find the new gene? They began with the fact that functionally important stretches of DNA will show signatures of evolution. A functionally unimportant stretch of DNA will acquire random mutations over millions of years. But if a segment of DNA has an important function, most mutations will be harmful. So the scientists compared non-coding DNA from chimpanzees, mice, and rat, for segments of DNA showed significant signs of negative selection. They identified 35,000 segments, all of which have resisted acquiring mutations for hundreds of millions of years. Then they looked at the human versions of each one. They found evidence that 49 of those regions had experience strong natural selection only in the human lineage. They ranked the DNA regions by the strength of natural selection and then investigated the ones at the top of the list. Lo and behold, they discovered that these DNA regions encoded genes that produce RNA, which turns out to do interesting things in the brain.

These scientists did not find a new gene and then try to make up a story to fit the theory of evolution. Evolution guided them to the genes. And they are hardly alone. Last year I blogged twice about scientists who find new genes and other important elements of DNA by looking for signatures of evolution. (Here and here.) Far from showing that “Darwinism is doomed,” the new research shows just how vital evolution is to understanding how the human genome works.

Last week I caught some of the talks at this year’s Dwight H. Terry Lecture at Yale. The lectures are in their hundredth year, and this time around the topic was “The Religion and Science Debate: Why Does It Continue?” The speakers include Ken MIller, talking about his experience at the Dover intelligent design trial, and Ronald Numbers of the University of Wisconsin, the leading historian of the anti-evolution movement in the U.S. (I’ll be writing an introduction to the volume that comes out of the lectures.)

If you’re interested, you can watch videos of the lectures now, here.

Over the weekend I wrote about the natural history of the Escherichia coli strain that has contaminated spinach. According to reports today, 109 people have been identified as sickened with Escherichia coli O157:H7, and one has died. In the comment thread of my post, the subject of antibiotics came up. It turns out that antibiotics are the last thing you want to take if you get sick with Escherichia coli O157:H7. It may turn a nasty–but temporary–case of bloody diarrhea into fatal organ failure.

More below the fold…

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I’m gearing up for some autumn talks. First up: Notre Dame University University of Notre Dame. The title of the talk is, “The Darwin Beat: Reporting on Evolution in a Controversial Age.”

When: Thursday, September 21, 4 pm.
Where: Jordan Hall Auditorium, Rm. 101

More information here.

I’ll let you know about some more talks as they approach.

Don’t eat your spinach.

That’s the word coming today from the FDA: they want everyone to avoid bagged spinach until they can get to the bottom of a nasty outbreak of Escherichia coli O157:H7, a virulent strain that infects an estimated 70,000 people in the United States and kills about 60. A number of people have gotten sick in the new outbreak, apparently from eating contaminated spinach, and there’s been a report of one death in Wisconsin.

There’s a fascinating–albeit gruesome–backstory to this outbreak, which I’ve been researching for my next book, a portrait of Escherichia coli. Escherichia coli is regular inhabitant of the human gut (not to mention the guts of mammals and birds). You carry about a trillion harmless E. coli. E. coli has also become the model par excellence for understanding the nuts and bolts of life. Lots of Nobel Prizes were awarded for research on these fascinating bugs.

Over the twentieth century, scientists began to discover that some strains of Escherichia coli are not so nice. A group of strains called Shigella cause diarrhea, for example, killing over a million people a year. And new virulent strains keep turning up. In March 1982, 25 people in Medford, Oregon, developed cramps and bloody diarrhea. The doctors identified a strain of Escherichia coli in some of the patients. The strain could not be found among the records of the Centers for Disease Control. That had never happened before. Three months later, another outbreak occurred in Traverse City, Michigan. The source of the bacteria proved to be undercooked hamburgers that the victims had eaten at a McDonald’s restaurant. Scientists named the strain O157:H7–a code for its distinctive surface molecules–and began to hunt for it among the bacteria that had been isolated from patients in earlier years. Out of 3,000 strains collected from American patients, a single one proved to be O157:H7, isolated from a woman in California in 1975. Searches in Great Britain and Canada turned up seven more cases, none before 1975.

O157:H7 slipped back into obscurity for a decade. It emerged again in the mid-1990s in a series of outbreaks spread across the world. One outbreak in Washington State, spread in undercooked restaurant hamburgers, sickened 732 people in 1993. Four of them died. More outbreaks flared up in other countries. In Japan radish sprouts tainted with O157:H7 sickened 12,000 people in 1997.

The outbreaks mobilized a lot of scientists to figure out what in the world this pathogen was. It is one of many strains of Escherichia coli that live in cows and sheep, dwelling peacefully in their guts. About 28% of cows in the United States are estimated to carry O157:H7. It can get into people through contaminated meat thanks to bad butchering (a single crumb of undercooked meat carrying 100 bacteria is enough for a potentially fatal infection). The animals also release the bacteria in their manure, from which it can be spread to vegetables and fruits, perhaps by the wind, slugs, or flies. It is also the reason why you really must wash your hands if you visit a petting zoo.

Once it gets in our bodies, E. col O157:H7 starts causing serious trouble. It builds a needle that it can jab into the cells of our guts. Through it they inject a cocktail of molecules. One of the first of these molecules is a receptor, which inserts itself into the wall membrane of the intestinal cells. In other words, Escherichia coli makes our cells part human, part microbe. The receptor can take in more of the molecules Escherichia coli O157:H7 produces, which alter how the cell reads its genes. Over 2000 genes in the cell change their patterns of expression. Some genes make more proteins and others shut down.

As its genes are manipulated, the cell begins to behave oddly. The skeleton-like fibers that support the cell begin sliding over one another to create a new shape. A pedestal-shaped cup rises from the top of the cell, offering Escherichia coli O157:H7 a place to rest. The cell also begins to leak fluids, which rush past the microbes. Safely cradled on their pedestals, the microbes can absorb nutrients in the flow. They also release toxins that dislodge hemoglobin, the oxygen-ferrying molecule, from blood cells. O157:H7 needs iron to grow, and hemoglobin is an iron-rich molecule. As the host bleeds, the microbe pulls fragments of hemoglobin into its interior and pries the iron atoms free.

These changes cause blood diarrhea, but they are not the worst of Escherichia coli O157:H7′s symptoms. Sometimes a few of the bacteria swell with toxins and burst.Their toxins enter our own cells, where they jam up the cellular factories that build proteins. Unable to make new proteins, the cells die and burst open. These toxins can slip into the blood vessels lining the intestines and soon spread to other organs. The kidneys are especially vulnerable to their attacks.

How can the same species be so gentle and so nasty? It has evolved. Escherichia coli has diversified into different strains. These strains adapted to different ecological niches. In some cases that adaptation made them harmless to us, allowing them to just graze on sugar cast off by other bacteria in our guts. In other cases, that adaptation made Escherichia coli a killer. Many different changes gave rise to this evolution. In some cases, genes spontaneously mutated and provided an extra reproductive edge to a microbe. In other cases, Escherichia acquired genes from other bacteria. In many of those cases, the genes came in bundles, delivered by viruses that pasted themselves into its genome and then became integrated into their host. You can find related versions of much of Escherichia coli O157:H7′s equipment in other strains of E. coli and in other species of bacteria.

The evidence suggests that the ancestors of Escherichia coli O157:H7 and its disease-causing relatives branched off from the best known harmless strain, called K12, a few million years ago. But it acquired some of its most important equipment more recently than that. Here’s a paper that presents some of the latest evidence about how O157:H7 and its relatives began acquiring new things such as toxins starting about 50,000 years ago. But it may not have been evolving into a better human pathogen. Instead, it may have been adapting to the animals that became our livestock about 10,000 years ago. Some research even suggests that O157:H7 helps sheep fight off cancer-causing viruses. For some reason scientists don’t yet really understand, when it gets into us, its behavior causes disease instead of health. In other words, humans created the conditions–from the first herds to the latest giant ranches and slaughterhouses–that fostered the evolution of this scary beast. And in the past 30 years, changes in how we get our food have allowed O157:H7 to emerge as a serious threat to public health.

And this evolution has not stopped. New strains of E. coli that cause much the same disease as O157:H7 have emerged in recent years. They are aquiring viruses bearing genes for toxins and other important equipment for making us sick. Those viruses are floating around in our sewers in vast numbers, with about one percent carrying various version of the toxin genes.

So I for one will be laying off the spinach for the next few days, and spending some more time getting to know these strange creatures and how they came to be.

Update: Naturally, Tara Smith has more. And Mike too.

Update 9/18 1:30 pm: Why antibiotics are the last thing you want to take if you get sick with this bug.

Welcome to the club, Chris Mooney…

Chris Mooney is the author of the excellent book, The Republican War on Science. He examines big hot-button scientific issues of the day such as global warming, stem cell research, and, of course, evolution. It’s a polemic, to be sure, but a well-researched one. Over the past couple weeks I’ve been meaning to write a post here to let readers know that it has just come out in paperback, with some great updates since the hardback. But it’s been hard enough for me to find time to blog, period, and it seemed like Mooney was enjoying a good reception without the little help I might offer.

I finally got roused to write about Chris this morning, because he’s now experiencing that weirdest of experiences, an attack from the Discovery Institute. In the course of his book, Mooney chronicles how the Discovery Institute has promoted intelligent design. This morning the Institute came out with a 31-page document (pdf) written by one of their “program officers,” Casey Luskin. Luskin claims to expose Mooney’s “factual and logical errors,” and demands that he retract or rewrite his chapter on Intelligent Design.

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The comment thread over on my recent creationist-critique post has been very lively. A second creationist has joined in the fray, and I’ve posted a response.