Supermodel microbes? You bet. Check out this gallery of lovely, sometimes whimsical microbe colonies.

Many blog and Twitter readers may be acquainted with Jonathan Eisen, a biologist at UC Davis. In my latest Meet the Scientist podcast, I spend an hour chatting with Eisen about what you can learn by looking at the genomes of particularly weird microbes–from radiation-resistant critters to bugs that live in the guts of insects or on the bellies of deep-sea worms. Check it out.

In my latest podcast, I talk to Hazel Barton, a microbiologist who explores the bizarre biology of microbes that live in deep caves. Check it out.

My second podcast is now live. I talk to Dennis Bray of the University of Cambridge about cells as microscopic computers. I first came across Bray’s work while working on my book, Microcosm. I was looking for new work on how E. coli manages to figure out where to go when it doesn’t have a brain or even a single neuron. Before long, I came across Bray’s remarkable work on the sophisticated information-processing that goes on inside the bug.

In this week’s podcast I sound like I’m broadcasting out of a tin can (I’m getting that hammered out), but don’t let my distractions get in the way of listening to Bray. And if you’re interested in more details, check out his new book, Wetware: A Computer in Every Living Cell.

Uff da–quite a week!

Monday brought Radio Lab’s great take on parasites, which I was thrilled to be a part of.

Tuesday was newspaper day, with a story in the New York Times on the evolution of flowers.

Thursday it was the sexual brain, the subject of my latest column in Discover complete with a safe-for-work video.

Friday brought the new issue of Time to the newsstands, with an article of mine on the minds of dogs.

Now at the close of the week, let me lure you into a different dimension of the media: podcasting.

The American Society of Microbiology has asked me to take over a biweekly podcast of theirs called “Meet the Scientist.” In each episode I’ll be talking with one of the many scientists who explore biology’s vast invisible world.  For my first podcast, I spoke to Michael Cunliffe, one of the scientists I wrote about recently who studies the ocean’s skin of jelly.

I’m still getting my bearings in the podcast universe, so feel free to dispense free advice. I’m looking forward to talking to many more scientists who study infectious diseases, synthetic biology, microbial evolution, and much more.

And now, off to New York for an old-fashioned talk. With Powerpoint.

Having written a book about E. coli has made me a keen aficionado of E. coli ties and E. coli plush toys. But a glass sculpture of E. coli? Now that’s classy.

This beautiful piece of sculpture is the work of the artist Luke Jerram. Check out his web site for his entire Glass Microbiology project. Swine flu never looked so good.

(Hat tip to Stan Carey)

Nature offers suggestions for summer reading in the latest issue, and  Microcosm is on the list. Don’t worry–just because the book is about E. coli doesn’t mean they’ll have to close the beach:

What is life? Why do creatures cooperate? Why do living things die? Carl Zimmer, a leading writer on evolution, finds answers to these and other big questions in the most humble of places — the common gut microbe, Escherichia coli. In Zimmer’s hands, E. coli becomes a window on to the basic properties of life and the ways that complex living systems can arise and change.

Zimmer weaves a narrative through the main principles of evolution, genetics and ageing, with stories of the people who made major breakthroughs along the way. His simple way of explaining complex ideas and his fast storytelling pace make for delightful reading. Each chapter contains ‘wow’ moments about bacteria and the joys and travails of the scientists who study them. The result is a scientific detective story that left me with a new appreciation of the trillions of microbes that live on and inside my body.

The editors also asked me for a suggestion, and I offered up Newton and the Counterfeiter by Tom Levenson.  The rest of the list looks good too, although I will probably have to abstain. I am determined to finish War and Peace, a few pages at a time if necessary, in this lifetime. Or maybe the next.

My latest story for the New York Times has just gone online. It continues my string of stories in which I look at the familiar and find it deeply strange. The previous one was about fireflies. Tomorrow’s story is about the surface of the ocean. It turns out to be a deeply weird thing–a gelatinous biofilm inhabited by a peculiar menagerie of microbes that play a vital role in our own well-being.

Check it out.

Scientists tinker with my favorite bug  so that it can solve mathematical puzzles.

In my book  Microcosm  (which has just come out in paperback), I took great pleasure in all the things that something as tiny as E. coli can do. It can survive in frozen soils and stomach acid. It can can build intricate tails which it can then spin hundreds of times a second in order to swim. It can navigate away from the bad and towards the good. It can protect itself from overheating by making just enough protective proteins it needs, with thermostat-like precision. It can survive starvation by folding its DNA into a crystalline sandwich and powering down for months, even years in some cases. It can build microbial cities out of goo, and even commit suicide to help its fellow E. coli survive.

Yet I may have underestimated the brainless intelligence of E. coli. It may even be able to  predict the future.

E. coli has 4000-odd genes, which it can use in various combinations to meet the many challenges it faces. But it does not use all those genes to make proteins and RNA molecules all at once. That would not only be a spectacular waste of energy. Instead,E. coli turns some genes on and keeps others turned off, a bit like playing the keys of a piano. Proteins can clamp onto stretches of DNA near certain genes, for example, making it impossible for the microbe to read them and make the corresponding proteins. When those proteins fall off, or are pried away, the genes can be switched on. (Likewise, other proteins can clamp onto other stretches of DNA and speed up the reading of genes as well.)

One of the most important chapters in the history of modern biology was the discovery of these switches in E. coli. In later years, scientists discovered this basic on-off strategy at work (with lots of variations, of course) in the DNA of all living things.

The way in which E. coli‘s genes switch on and off is well-suited to its particular kind of life. For example, E. coli can make proteins that allow it to feed on lactose, the sugar in milk. But most of the time, it keeps the genes for those proteins shut down. If it should encounter lactose, however, the sugar molecule can pull away the repressing proteins, initiating a series of events that leads to E. coli producing a lot of lactose-digesting proteins.

In a case like this, E. coli is responding to something that’s already present in its environment. So-called “higher” species, like us, can also respond to signals of things to come. In fact, thanks to our brains, we can learn new signals. (Think of Pavlov’s dogs, drooling at the sound of the dinner bell.) That led scientists at Princeton to wonder whether E. coli can see into the future as well. It may not have a brain made up of billions of cells, but it does have a complex network of genes that might be able to use information to make predictions about things to come.

The Princeton scientists started by considering E. coli’s natural history. You get regularly infected with new E. coli carried from your hands to your mouth. (Fortunately, the vast majority of these bacteria are totally harmless. Just remember, don’t eat raw cookie dough!) For the E. coli that’s just arrived in your mouth, the world begins to change. It immediately gets a lot warmer, for one thing. Later, as it moves from your mouth down through your gut, the level of oxygen in its environment will drop to near zero. In order to survive, E. coli has to shut down the network of genes it uses to metabolize sugar with the help of oxygen, and then switch on hundreds of other genes for feeding without oxygen.

A sudden rise in temperature is a reliable signal that oxygen will start to drop over the next few hours. The Princeton scientists wondered if  E. coli might use it as a cue to start to prepare for the change. To find out, they experimented on some  E. coli, keeping careful track of which genes were turned on and off when they tweaked the temperature and oxygen levels. It turns out that when E. coli gets warm, it not only switches on heat-defense genes, but also starts making the switch to low-oxygen genes. This switch is remarkable when you consider that it can happen while  E. coli is bathing in a broth rich in oxygen. Unless the oxygen is going to drop soon, this would be a disastrous decision.

It was possible, though, that  E. coli has to switch to a low-oxygen program whenever it defends itself against high temperatures. To test that possibility, the scientists turned  E. coli‘s world upside-down. They periodically raised and lowered both the oxygen levels and the temperature in flasks of  E. coli. But now a rise in temperature was followed 40 minutes later by a rise in oxygen, not a drop.

The scientists allowed the bacteria to grow and reproduce for hundreds of generations in this bizarro world. Mutations arose, and beneficial ones spread through the population thanks to natural selection. The scientists then took a look at the bacteria after they had adapted to the new pattern of temperature and oxygen.

Now a rise in temperature prompted a far weaker response from the genes  E. coli uses to survive at low-oxygen levels. The bacteria with mutations that allowed them to continue using oxygen outcompeted the ones that automatically made the switch when the temperature rose. Their experiment suggests that the programs the bacteria use to survive high temperatures and different levels of oxygen are not inextricably linked. The link must be an adaptation, the scientists argue. At some point in the past, the ancestors of E. coli evolved the microbial wisdom that a rise in temperature foreshadows a drop in oxygen.

The Princeton scientists published the details of their experiment a year ago. Now, in the current issue of Nature, a team of Israeli scientists offer evidence that E. coli predicts the future in another way.

The Israeli scientists noted another reliable clue E. coli gets on its journy from mouth to gut. Thanks to the chemistry of our intestines, the upper part of the digestive tract has lactose on offer, but further down in the gut, another sugar called maltose is available. The Israeli scientists wondered E. coli “know” that if it encountered lactose, maltose would be coming soon.

First, they looked at which genes switched on when they fed E. coli different kinds of sugar. Feeding it maltose caused it to make a lot of proteins for digesting maltose. But feeding it lactose caused it not just to make lactose-digesting proteins, but low levels of proteins for digesting maltose too. The effect did not go in the other direction, though. Feeding E. coli maltose does not cause it to make a lot of lactose-digesting proteins.

The Israeli scientists then ran an experiment to see if there was any advantage to E. coli making the maltose proteins in response to lactose. There is indeed. Bacteria that are first exposed to lactose actually grow faster on maltose than bacteria that feed on maltose alone. Other sugars can’t give E. coli this priming advantage. Nor does the advantage work in reverse. Exposing E. coli to maltose does not speed up its growth on lactose.

Finally, the Israeli scientists ran an evolution experiment of their own. They fed E. coli high levels of lactose without any maltose. Under these conditions, making maltose-digesting proteins in response to lactose is a waste of energy. After 500 generations, the scientists found, the bacteria stopped making maltose proteins in response to lactose (although they could still make them in response to maltose itself).

E. coli does not actually learn to make associations the way Pavlov’s dogs learned. The neurons in the brains of the dogs altered their connections. E. coli evolves new connections between its genes over the course of hundreds of generations, as mutations offer up new arrangements, and natural selection favors the ones that speed up the bacteria’s growth. But these experiments do illuminate some of the interesting ways in which evolution resembles learning.

The commentary that accompanies the new paper has the clever headline, “Microbes exploit groundhog day.” In the movie Groundhog Day, you may recall, Bill Murray wakes up day after day only to find that it’s still February 2. After a while, he starts to look clairvoyant to the people around him, because he can anticipate everything that’s going to happen. In some respects, life is a lot like Groundhog Day. Things repeat themselves in a predictable order. Perhaps body temperature and low oxygen are like Groundhog Day for E. coli. Perhaps lactose and maltose are too.

But, of course, a lot of life is not like Groundhog Day. In many cases we can’t predict the future, and so we can’t know exactly what to do now to be best prepared. The same goes for E. coli. So what does E. coli do?

It pretends that it’s betting on horses.

But to find out how it does that particular trick, you’ll have to read about it in  Microcosm.

(Did I mention that it’s now out in paperback? Did I mention how the Boston Globe called it “quietly revolutionary,” and how other people have said equally nice things about it? Just asking…)

Last week, three teams of scientists published three massive studies in Nature on the genes behind schizophrenia. They scanned thousands of people to find variants of genes that tended to show up more in people with schizophrenia than in those without it. And they found a heap of genes. There are thousands of different variants that each may raise your risk of schizophrenia by a tiny amount.

Nicholas Wade, a veteran genetics reporter at the New York Times, has been following the quest to trace diseases to genes for a long time now. And when Wade tried his hand at blogging last week, he laid down a harsh verdict.

Press releases from five American and European institutions celebrated the findings, one using epithets like “landmark,” “major step forward,” and “real scientific breakthrough.” It was the kind of hoopla you’d expect for an actual scientific advance.

It seems to me the reports represent more of a historic defeat, a Pearl Harbor of schizophrenia research.

By “defeat,” Wade was not saying that the research was wrong. It was just not going to lead to any quick fixes for this devastating disease. While the risk of schizophrenia can be inherited, that does not mean that you can take a pill that compensates for a single broken gene and cure it.

These new results are depressingly similar to a string of searches for the genes linked to other conditions, such as diabetes and high blood pressure, as I explained in my recent essay for Newsweek, “The Gene Puzzle.” Now that scientists can read the human genome and scan thousands of people’s DNA, they’re not finding easy answers. They instead are finding networks upon networks of thousands of genes, that can be disturbed in a staggering number of ways.

It can be frustrating to discover just how complex our genes can be. But we really shouldn’t be too surprised. We’ve had plenty of warning about the complexity of life from a much simpler organism: E. coli.

E. coli only has 4,000 or so protein coding genes (we’ve got about 20,000, plus thousands of other important chunks of DNA). E. coli doesn’t have to develop into a brain or a heart or a toenail: all it needs to do is be E. coli, a single, tiny cell. As I explain in my book Microcosm: E. Coli and the New Science of Life, E. coli has been studied up and down and every which way for a century. It is the best-understood species on Earth. And by 1973, the great biologist Francis Crick, co-discoverer of the structure of DNA, decided  E. coli should be the subject of a singular scientific project–a kind of biological moon shot. He called for the “complete solution” to E. coli: a total explanation of how the cell sustained itself, grew, and reproduced.

It’s been 36 years since Crick’s call, but scientists have yet to figure E. coli out. For one thing, they don’t have a very good idea of what a lot of its genes are for. According to a study published in PLOS Biology in April, the function of a third of  E. coli‘s genes are uncharacterized. The authors of that study were able to come up with hypotheses for what all those 1431 genes do, but they are rough hypotheses at best. The scientists proposed the some genes are involved in building proteins, for example, or constructing membranes. They could not offer a detailed explanation for how the structure of each of those proteins allowed it to carry out some particular function.

It will take a lot of scientists doing a lot of experiments to figure out exactly what those 1431 genes are doing. And conversely, it will take a lot of work to figure out the interactions of genes that produce even the simplest things about E. coli. This diagram comes from a paper published last month in Molecular Systems Biology on one such simple thing (click on it for a bigger view). Scientists have been engineering E. coli to make an alcohol called isobutanol, which might serve as an alternative fuel. The only catch is that isobutanol is poison for E. coli. Even a tiny amount of the stuff will cause the bacteria to stop growing, which is the last thing you want to happen to microscopic fuel factories. So scientists at UCLA tried to figure out how isobutanol makes E. coli sick. This diagram sums up what they figured out: a single kind of molecule can trigger all kinds of changes in the activity of a number of proteins, and those changes cascade through the cell, as proteins shut down genes for other proteins or activate other ones.

That being said, the scientists did figure out the answer to this particular question, and they are figuring out how to tweak this network to help E. coli survive its self-made poison. While E. coli should make us skeptical of big promises about mastering the human genome in the near future, we can still have some hope for the distant future. Pearl Harbor, after all, did not end the war.

Next week the paperback edition of my book Microcosm: E. Coli and the New Science of Life will be published. In the book I approach E. coli as a microscopic oracle that can reveal great secrets about how life in general works. This is not actually a rhetorical stretch; over the past century scientists have put a spectacular amount of work into understanding this bug. And, as I write in the book, E. coli continues to offer surprises. In celebration of the arrival of the paperback Microcosm, I’m going to take a look at some fresh-out-of-the-oven research on E. coli that may change the way you think about life as a whole.

There’s no better way to kick off Microcosm Week than with some chocolate chip cookies. Or, to be specific, some raw cookie dough carrying a dangerous cargo of toxic E. coli.

The name ” E. coli ” embraces a veritable empire of bacteria. While all E. coli share the same backbone of certain genes, they can be divvied up into a vast number of strains, each with a distinctive genetic profile. Many of those strains are harmless. You have a couple dozen strains of  E. coli dwelling inside you right now, quietly grazing on the extra sugar in your gut. But some strains are extremely nasty. One strain, known as E. coli O157:H7, can stick to the walls of the intestines and build needles through which it can inject molecules into host cells that can alter them in many ways, so that the cells disgorge food the microbe can eat. Typically this manipulation leads to painful, bloody diarrhea but little more. On rare occasion, however, the bacteria unleash toxins that can spread through the blood stream, killing cells and leading to kidney failure.

At the end of June the Centers for Disease Control detected E. coli O157:H7 in a batch of Nestle chocolate cookie dough. It’s a mysterious new move from a mysterious microbe. The normal host of  E. coli O157:H7 is livestock–especially cows and sheep. In those animals, this strain doesn’t seem to do much harm and may even benefit its host. Studies on the evolution of E. coli O157:H7 suggest that it emerged and spread in parallel with the spread of cattle over the past 1000 years. The bacteria can spread from cow to cow by passing out of one host with their droppings. The bacteria can survive for months in a barn or a corral, and can then get blown onto grass or other food eaten by another cow. People can get sick from an infected cow if its intestines are nicked during slaughter and the bacteria can contaminate the muscle. That’s why you should always cook hamburgers all the way through–just a few microbes are enough to get you sick.

Yet some of the worst outbreaks of E. coli O157:H7 have not been caused by tainted beef. In 1996, for example, radish sprouts contaminated with E. coli O157:H7 infected thousands of school children in Japan. And now the bacteria have turned up in cookie dough. There’s no official word for how the bacteria got from a cow to a cookie (or at least, a cookie in the making). But chances are good that the story is going to be complicated, in a way that’s both disturbing and fascinating.

I base that prediction on the last headline-making E. coli outbreak, in 2006. Then it was spinach that was ferrying the bacteria, not cookie dough or sprouts. Over the course of two months, 205 people got sick from tainted spinach, and 15% of them developed the more dangerous form of the infection (called hemolytic uremic syndrome). That was over three times the average rate in previous outbreaks, and so scientists have taken a closer look at these particular bacteria–this sub-sub-strain, as it were, to figure out what made it so nasty. The scientists published their preliminary results last year (about which I wrote a piece for Slate), but now they’ve just published their detailed analysis in the journal Infection and Immunity.

The new study drives home a remarkable lesson: the bacteria that caused the spinach outbreak was different in many ways from other E. coli O157:H7. It changed in two ways.

Way #1: New mutations arose spontaneously in individual microbes, were passed down from ancestors to descendants, and then spread through the population by natural selection or a more random process called genetic drift. These mutations altered genes that carry out many functions in E. coli, from the chemical reactions it uses to break down food to the shape of its membrane. It also has mutant genes for cellulose and for hair-like projections from its surface, both of which have proven important to E. coli O157:H7′s ability to stick to surfaces, like those of sprouts.

Way #2: It turns out there are also a lot of genes in the spinach outbreak bacteria that are not found in any E. coli O157:H7. Some aren’t even found in any other E. coli. These genes did not evolve through the familiar rise of new mutations in old genes. Instead, the bacteria picked them up from other species at some point in the past few years. Viruses, for example, can accidentally pick up genes from one host and then insert them in the genome of a different host.

The genes acquired by the spinach E. coli include one encoding a protein that can twist the DNA in your cells so that they can’t send out alarms to your immune system. Another imported gene allows the bacteria to suck in the iron-bearing molecules in your blood. And two other genes bears a striking resemblance to a pair of genes found only in a species of bacteria that grows on plant roots.

Those genes are particularly interesting. The plant-dwelling bacteria uses their genes to manipulate the biology of their plant hosts, such as stimulating the roots they live in to grow. It’s possible that when the spinach E. coli picked up these genes, they helped the bacteria thrive by letting them grow on plants. In other words, this particular kind of E. coli didn’t just get swept away from its ordinary home inside a cow. Along with genes for living inside mammals, it has also picked up genes that help it live on plants. And it made that transition only very recently.

We’ll have to wait to see if the cookie E. coli has evolved its own peculiar set of genes. But as I write in Microcosm, this kind of evolutionary history–a mix of mutations handed down through the generations along with genes moving from one species to another–is hardly unique to a few outbreaks of food poisoning. In fact, these intertwined processes have been shaping life, our own included, for billions of years.

[If you want to read some reviews of Microcosm: E. Coli and the New Science of Life, I've posted a collection here.]