Princeton biologist Bonnie Bassler studies the chemical conversations bacteria use to work together and (sometimes) to make us sick. She joined me for my latest podcast, bringing her trademark enthusiasm and rare skill at telling a good scientific story. Check it out.

And if you crave more, check out her excellent TED lecture last year.

36,000,000,000,000,000,000,000,000,000,000 is a big number. But that’s actually the number of microbes in the ocean. How on Earth do you comprehend that monstrous menagerie? In my new Meet the Scientist podcast, I talk to pioneering microbiologist Mitch Sogin about a major new project to census the sea’s microbial diversity. Check it out.

Could E. coli some day take the place of deep sea oil wells? In my latest podcast I talk to James Liao of UCLA about engineering microbes to churn out high-performance fuel. Check it out.

Bacteria and other microbes suck up and blast out vast amounts of greenhouse gases. Over at Yale Environment 360, I take a look at how they will behave in a world warming up as we inject carbon dioxide into the atmosphere. Will they draw down some of the extra CO2, or will the heat spur them to spew out more? Or both? The answer isn’t clear yet, but it’s important. After all, it’s a microbial planet, and we just live on it. Check it out.

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If you’re at ASM, I just want to let you know I’ll be at the ASM Press Bookstore from 1 pm to 2 pm on Wednesday. The bookstore is on the far right end of the lobby as you’re standing in front of the convention center. If you want to talk about the things I’ll be discussing this afternoon at 5:30 pm, come by. Also, ASM Press has signed copies of Microcosm for sale. See you there!

I’ve got some public face time coming up:

Tuesday, May 25, 5:30 pm: In San Diego, I’ll be talking at the American Society for Microbiology. I was asked to speak at the President’s Forum, “Tell the Story of Science.” My own talk is, “Newspapers, Blogs, And Other Vectors: Infecting Minds With Science In the Age of New Media.”

Random House will be kindly providing copies of Microcosm for sale at the meeting. I will spend some time signing them all when I get to the conference Monday. The books will be available at the American Society for Microbiology Press Booth. (I’ll update this post when I know exactly where the booth is located.)

I’ll also plan on hanging out at the booth at some point on Wednesday, hoping that I can meet face to face with some of the Loom’s microbiologist readers. (Again, I’ll update this post about exactly when I’ll be there once I get to the meeting.)

Thursday, June 3, 7 pm: The World Science Festival returns to New York for its third year, and I’m delighted to enter my third year of moderating panels for them. I’ll be part of “Modern MacGyvers,” a gathering of innovative thinkers who are designing solar panels for camels, cook stoves that could save millions of lives, and other important inventions.

I may be asked to moderate other panels; if so, I’ll update this post accordingly. I will definitely be going to some other sessions as an audience member: the line-up looks great.

Thursday June 3, 8 pm and 10 pm: The Science Channel is airing, “Creating Synthetic Life,” a show about Craig Venter’s new hand-made cell. The producers asked me to talk about the research Craig Venter and his team have been carrying out for the past fifteen years on the path to creating artificial life. At the time they interviewed me (a few weeks ago), I knew there was some big news coming down the pike, but wasn’t able to talk about the particulars. So I expect that I’ll turn up on the show speaking in hazy generalities set in the future tense. Feel free to set your TV on mute when I show up. But based on the previews, I think the rest of the show is worth checking out.

Craig Venter has taken yet another step towards his goal of creating synthetic life forms. He’s synthesized the genome of a microbe and then implanted that piece of DNA into a DNA-free cell of another species. And that…that thing…can grow and divide. It’s hard to say whether this is “life from scratch,” because the boundary between such a thing and ordinary life (and non-life) is actually blurry. For example, you could say that this is still a nature hybrid, because its DNA is based on the sequence of an existing species of bacteria. If Venter made up a sequence from scratch, maybe we’d have crossed to a new terrain.

Anyway–this news just hit the wires thanks to an embargo break, so I don’t have time to go into more detail. Joe Palca at NPR has posted his article on the subject. For background, please check out these stories I’ve written about this general area of research:

Tinker, Tailor: Can Venter Stitch Together A Genome From Scratch?

The Meaning of Life

The Six Most Important Experiments In The World

Artificial Life? Old News.

The High-Tech Search For A Cleaner Biofuel Alternative

On the Origin of Tomorrow

My Bloggingheads interview with Venter

Update: The scientists are in a live press conference that started a 1 pm.

Less than two percent of the human genome is made up of protein-coding genes. Fifty years ago, scientists launched an expedition of the other 98 percent. It has been a slow march for much of that time, but in recent years the pace has picked up, thanks to advances such as new ways to sequence DNA. Scientists are now generally agreed that some of the non-coding DNA falls into several categories, including

–sites where proteins can bind in order to switch nearby genes on and off

–genes for RNA molecules. Instead of just serving as a template for turning genes into proteins, RNA actually plays lots of roles in the cell, such as sensing levels of different molecules in the cell and interfering with other RNA molecules to control levels of protein.

–old viruses and other genomic parasites. Some viruses can insert their genetic material into our genomes so that it becomes a permanent part of our DNA.  These viruses and other parasitic stretches of DNA can, from time to time, make copies of themselves, which then get inserted back into the genome. In a few cases, these genomic parasites may be domesticated, evolving to do valuable things like help build placentas or fight off viruses. But for the most part they’re either useless or downright harmful–just like any other source of mutation.

–Hobbled or dead genes. Sometimes mutations strike genes so that they can no longer produce proteins. Sometimes these mutations are fatal. Other times, we’re able to survive without a particular gene. The pseudogene, as it’s known, may linger on in the genome for millions of years. In a few cases, pseudogenes may still be able to produce useful RNA molecules. But for the most part, they’re just baggage.

The first two categories include stretches of DNA that are useful. The second two include stretches that are useless. Now comes the hard part: figuring out just how much of the genome is made up of each. The question goes beyond mere census-taking, because it will help us understand how the genome works, in its entirety. And it will also reveal how much of the genome provides no benefit at all.

I wrote an article about this line of research for the New York Times in November 2008. I described some scientists who were betting that most of the genome wouldn’t be good for much, and others who believed that most of it was serving important functions. The latter group pointed to studies in which scientists tallied up all the RNA transcripts produced by one chunk of the genome. They found that most of the DNA they analyzed produced RNA. John Mattick, a member of the research team who works at the University of Queensland in Australia, claimed that most of that DNA encoded useful molecules. “My bet is the vast majority of it — I don’t know whether that’s 80 or 90 percent,” he said.

But it was just a bet. A lot of work remained to figure out what all that RNA really signified. This week scientists at the University of Toronto published a study that suggests, contrary to Mattick, it’s full of sound and fury, signifying nothing. They used new methods to survey the RNA produced by the genome and compared their results to the ones from older methods. They found that most of their RNA came from regions of the genome that are already known to be protein-coding genes. Very little RNA came from elsewhere in the genome. They argue that the older methods were crude, so studies based on them were loaded with false positives. Protein-coding genes are not the only source of RNA transcripts in the genome, but a lot of the extra ones may just be the result of sloppiness. When proteins slide down DNA, making RNA transcripts, they sometimes grab onto the wrong stretches. The extra RNA gets broken down quickly–as useless and as inevitable as sparks flying off a grinding wheel.

Nature News has a nice write-up, as does PLOS Biology (from which I shamelessly lifted my Macbeth).

[Image: MIT]

In 1991, a 21-year-old Finnish computer science student named Linus Torvalds got annoyed. He had bought a personal computer to use at home, but he couldn’t find an operating system for it that was as robust as Unix, the system he used on the computers at the University of Helsinki. So he wrote one. He posted it online, free for anyone to download. But he required that anyone who figured out a way to make it better would have share the improvement with everyone else who used the system. Torvalds would later tell Wired that his motives were not noble. “I didn’t want the headache of trying to deal with parts of the operating system that I saw as the crap work,” he said. “I wanted help.”

In his quest to avoid crap work, Torvalds unleashed a monster. People began to download the system, dubbed Linux, all over the world. Within a few weeks, Torvalds was getting emails from hundreds of users, explaining how to fix bugs and how to add new bells and whistles. People began to write programs that would only work on Linux computer. They founded companies around Linux-based software. Millions of people chose Linux for their computers, and major computer companies like Microsoft and Dell begn to support the system. Along the way, Linux evolved. Torvalds’s first version contained 10,000 lines of code. Linux now holds over 12 million lines.

Those 12 million lines may seem like a hopeless thicket of code, but it actually has a hidden structure. It’s divided up into chunks, each of which carries out a particular task. All told, they carry out 12,391 separate functions. The functions are also connected. If Linux carries out one function, the system will direct the computer to carry out other functions. You can think of Linux as a network, with the functions joined together by links of control. Computer programmers can map out that network as a so-called “call graph.”

Linux bears an uncanny resemblance to the genes in a living cell. Many genes make proteins that act as switches for other genes. The proteins clamp onto DNA near a target gene, allowing the cell to read the gene and make a new protein. And that new protein may, in turn, grab onto many other genes. Thanks to this hierarchy of switches, cells can respond to changes in their environment and quickly carry out complex behaviors, such as reorganizing themselves to feed on a new kind of food.

A number of scientists have begun to compare natural and manmade networks. A lot of the same rules appear to be at work in the growth of the Internet, airport connections, brain wiring, ecosystem food webs, and gene networks. But very often, scientists are finding, it’s the differences between natural and manmade networks that are most revealing, offering clues to the different ways in which people and evolution build complex things.

In the Proceedings of the National Academy of Sciences this week, Koon-Kiu Yang of Yale and his colleagues present the first detailed comparison of Linux’s network to a gene network. (The paper will be here.) Thanks to the open-source nature of Linux, the scientists could look at every line of code in every version of the system over the past two decades, from Torvald’s first primitive stab to its current sophisticated form. And for a living cell, Yang and his colleagues turned to the living equivalent of Linux–a biological network they could analyze from top to bottom. They chose E. coli. coli, since it is the best-studied species on Earth. (Why E. coli? There’s a certain book that will explain it to you.)

Over the past fifty years, scientists have mapped 1,378 interactions among E. coli genes. Out of that research, Yang and his colleagues built a microbial call graph. They assigned each gene to one of three categories. If a gene switched on one or more genes, but was not itself switched on by another gene, they called it a “master regulator.” If a gene was switched on by a different gene and then, in turn, switched on other genes, the scientists dubbed it a “middle manager.” And if the gene was switched on but did not then switch on any other genes, they called it a “workhorse.” The scientists drew the network of master regulators, middle managers, and workhorses.

The scientists sorted all the functions in Linux by the same rules. Here is the picture that emerged.

(N.B.: for the sake of clarity, the scientists only used 10% of the nodes in the full Linux call graph. But the complete picture would look the same.)

Both Linux and E. coli are organized into hierarchies. But their hierarchies have different shapes. E. coli‘s genome is dominated by workhorses. Middle-managers and master regulators make up less than 5% of the total number of genes. In Linux, by contrast, over 80% of the functions are in the upper echelons. Each workhorse in Linux is controlled to many middle managers. In E. coli, on the other hand, each workhorse gene is typically controlled either by a few genes or just one. And so in E. coli it’s the higher levels where genes have the most links, not the workhorses.

Once Yang and his colleagues had drawn the two networks, they looked at the paths information takes as it flows from master regulators down to workhorses. E. coli’s genes are organized into relatively distinct modules. When a master regulator swings into action–in response, say, to a spike in temperature–it switches on a set of other genes with relatively little overlap with the genes switched on by other master regulators. Linux, by contrast, has blurry boundaries. Four out of five Linux modules overlap, in contrast to 5% of E. coli‘s.

The networks in E. coli and Linux don’t just look different. They also grew in different ways as well. The oldest genes in E. coli‘s network–the ones shared by many other species of microbes–are its workhorses. The genes higher up in the E. coli hierarchy have emerged more recently. Those higher-ranking genes have also been undergoing a lot of evolutionary change since they first emerged. The old genes, by contrast, have changed little.

The history of Linux has played out differently. A lot of the oldest functions in Linux are middle managers or master regulators, not workhorses as in E. coli. And while old genes in E. coli haven’t evolved much, programmers have heavily rewritten Linux’s old functions.

Both networks developed, step by step, as increasingly sophisticated systems for operating things–computers or cells. But the Linux network was the work of programmers, while E. coli is the product of four billion years of evolution. The differences in the history and shape of the two networks emerge from the ways in which they developed. The programmers who built Linux did not have the time to invent entirely new workhorse functions. It was simpler for them to just use the old workhorse functions in new modules. But this strategy leaves Linux a lot more fragile than a biological network. Its modules overlap, so that in many cases, a workhorse function is essential for many different modules at once. As a result, Linux gets buggy and prone to crashing. And so as programmers improve Linux, they’ve had to fine-tune its all-purpose functions at every step of the way.

E. coli is far more rugged. Mutations crop up all the time as the bacteria multiply, and yet they generally don’t suffer a catastrophic network crash. One reason E. coli is so robust is that its modules have evolved to be distinct. Overlapping modules make cells particularly vulnerable to mutations, because a single mutation can shut down a lot of their essential biology. Natural selection favors organisms with a more rugged network.

Because E. coli is the product of evolution, rather than of programmers, parts of its genome have changed relatively little over billions of years. The oldest parts of the network are the workhorse genes–the ones that encode primitive proteins that do the fundamental work of life, like building new pieces of DNA. They can tolerate very little change. It’s much easier instead for E. coli to evolve new ways of controlling those workhorses.

This kind of comparison is very new, and it’s not clear yet what scientists will find when they compare Linux to other genomes–particular to the genomes of more complex species like ourselves. E. coli has only about 4300 genes. We have 20,000 protein-coding genes. A lot of those genes control other genes. Indeed, a typical human gene has a lot of switches, all of which have to be thrown in order for the gene to make a protein in a certain situation. The human genome is also packed with thousands of genes that don’t encode proteins, but which may encode RNA molecules that also switch genes on and off. Scientists just don’t know enough yet about the human genome to map its network the way they’ve mapped E. coli. But it’s possible that when they finally do, it will be a lot more top-heavy, with a lot more overlapping modules and multi-tasking workhorses.

If that turns out to be the case, biologists will have a new question to keep them busy for a long time to come: how did Linus get to be so much like Linux?

[Update: Fixed Torvalds's name and other typos. Thanks for the proofing!]

What will the world be like when your genome sequence costs less than a cell phone? A couple days ago I went to Cambridge, Mass. to find out.

The occasion was a meeting called “Genome, Environments, and Traits,” or GET for short. The history of the meeting is in the upper ranks of my list of meetings with strange histories. In 2006, the Harvard geneticist George Church (arguably the smartest, most influential biologist you never heard of) decided to launch a new kind of human genome project. At the time, scientists had only published the sequence of a single human genome, at a cost of $3 billion. And for all that money, the genome was actually a gap-riddled patchwork from several individuals, and only included the DNA from one copy of each pair of chromosomes. Church declared that he would gather the sequenced genomes of 100,000 individuals, along with information about their health, and make all that information available for scientists to study in order to learn more about human biology. Church issued a manifesto of sorts in Scientific American, called “Genomes for All,” which you can read here (pdf) and also talked to Emily Singer of Technology Review here.

To kick off his Personal Genome Project, Church sequenced his own DNA, put it online, and promptly got a message from a doctor on the other side of the country, informing him that he should adjust his cholersterol medication. Church also persuaded nine other people to volunteer to have their genomes sequenced and laid out online for all to see. One of those first ten, the Harvard psychologist Steven Pinker, helped spread the word with this article that in the New York Times Magazine in 2009.

Those early sequencees got together from time to time to talk about the project and their own experiences contending with having a genome available for all to see. This genomic club was an intimate one at first, but its membership is now exploding. With each passing month, the cost of genome sequencing is crashing, companies are gearing up to sequence genomes on a commerical scale, and scientists are starting to think seriously about looking at complete genomes as a regular part of clinical practice. For this year’s meeting, Church decided to try to get as many people with sequenced genomes as possible altogether in one room. It would probably be the last time such an exercise would be possible.

I got pulled into the fun when my phone rang a couple months ago. On the line was Robert Krulwich. Krulwich is the co-host of the show Radiolab, covers science for NPR and ABC News, and is also the go-to guy for live–and lively–interviews with towering figures of science. (Observe him handle both E.O. Wilson and James Watson at once–a bit like juggling torches while riding a unicycle. He doesn’t break a sweat.)

Church had asked Krulwich to come to the meeting and moderate a discussion of a dozen or so sequencees that would take up the first three hours of the meeting. Krulwich decided this was a two-person operation. Wise move. This was heavy lifting.

It would be absurd to have everyone one the stage the whole time, so we came up with a scheme to move people quickly from the front row of the audience to the stage, playing a genomic game of musical chairs. Making it even more challenging was the fact that we had such big subjects to talk about, from the development of next-generation sequencing to the application of genomics to genealogy to the issues of privacy that genome sequencing raises.

And then there was the matter of the line-up. Any one of the speakers could have held the stage on his or her own for an hour. It felt very strange whisking Henry Louis Gates onto the stage and then whisking him off. This, after all, is a guy who can hold an entire TV series together. At the meeting, he talked about getting his father’s genome sequenced as well as his own–becoming the first father-son team to do so. A comparison of the two genomes allowed him to see fifty percent of the genome of his deceased mother–an experience that felt like seeing her come back to life. Gates talked about the experience of seeing so much European DNA in his genome. If you look at my lab results, he said, I’m a white man.

–Well, we’d love to hear all about it, Professor Gates, but we’ve got to move on! A round of applause everyone, and let’s move those chairs!

Krulwich and I also struggled with the challenge of talking about genomics with people who are so uniformly gung-ho about it that they’ve had their genomes sequenced–and of talking to those sequencees in front of an audience made up of genome scientists, people from the biotech sector, venture capital folks, and other assorted people who are, shall we say, already in the genomic tank. Neither Krulwich or I received a fee for our involvement in the meeting, and we were not about to join the ranks those miserable fake journalists you see on infomercials late at night, pitching pre-scripted softballs like, “So tell me again how your company is going to become a raging success in the personal genome business.”

Krulwich and I therefore tried, politely, to nudge the sequencees out of their comfort zone. How on Earth, I wondered, could the sophisticated analysis of genomes become a regular part of everyday medicine when most doctors have office full of old paper records? Was it fair to children to get their genomes sequences when there was nothing immediately wrong with them? What good is getting your genome sequenced if all you get is a laundry list of genetic variations that have obscure relationships to all sorts of diseases that you may or may not get? How can there be a business in genomes if, as Church predicts, the cost of genome sequencing will be dropping to, essentially, free?

In many cases, questioners and answerers ended up talking past each other. Krulwich asked James Watson what he thought about the ethical concerns about genome sequencing. His answer: “Crap.” The other sequencees were more polite when we asked questions that seemed irrelevant to them. When Krulwich asked sequencee Esther Dyson about the potential risks of getting her genome sequenced, Novocell CEO John West pointed out that she was preparing to go to the Space Station. Why were we obsessing about the risks of Dyson’s genome, with no apparent concern that she was about to have herself shot into space on the tip of a rocket?

I think the best answers were deconstructions. Consider this: Widespread genome sequencing will make it possible to test babies for genes associated with intelligence. Isn’t that a horrible thing?

At the meeting, Church pointed out that we already test for intelligence genes, and nobody gets outraged at all. Babies are routinely tested for a genetic disorder known as PKU, in which children are born unable to break down an amino acid called phenylalanine. Phenylalanine builds up to toxic levels in the body, leading to mental retardation. But the mutation that causes PKU does not necessarily cause PKU. Genes are not destiny. If children keep a diet low in phenylaline, they end up with normal intelligence. Knowledge of our genome is not sinister in this case. Ignoring the facts of PKU would be the sinister thing to do.

Church is right, but the story of PKU only carries you so far into the future of genomic medicine. PKU is a rare disorder, affecting an estimated 1 child out of every 13,500 to 19,000 births. It’s also unusual in that it’s caused by the failure of a single enzyme. A single mutation to a single gene is enough to cause it. And the fact that it can be so readily treated is also unusual. Cystic fibrosis, for example, is another single-gene disease. Despite the discovery of its genetic basis 20 years ago, doctors have no cure to offer CF patients.

The genetic roots of common disorders, like high blood pressure and Alzheimer’s disease, have proven to be a lot more complex. It’s possible that the risk for some common diseases may be the result of variations on hundreds of genes, with each variation contributing a tiny fraction of the risk, and different combinations able to cause just as much of the disease. It’s also possible that the risk for some diseases is due to very rare mutations, each of which has very strong effects. There may be a lot of these rare mutations in the world’s population, making it hard to find them all and figure out what they do.

The sequencees at GET didn’t avoid this messy reality. In fact, one of them embodied it. James Lupski, a Baylor College of Medicine geneticist, suffers from a hereditary disease called Charcot Marie Tooth Disease, in which the coating of the long nerves in the limbs starts to fray. He has had to have operation after operation on his feet to treat the symptoms. Lupski studies the cause of the disease, and recently he had his genome sequenced to find its source. He turned out to have some mutations that have been linked to Charcot Marie Tooth Disease before, but he and his colleagues also found a new gene, with a different mutation in his mother’s and father’s copy. The discovery did not point immediately to a cure; instead, it added to the complexity of the disease. Lupski explained his own disease and his difficult research on it in unsentimental detail. Science is hard, Lupski said, and anybody who thinks it isn’t is fooling themselves.

It was too bad that the meeting didn’t take place next week instead of this week. Today, the Lancet published a genome paper that included among its co-authors two of the sequencees we spoke with: George Church and Steven Quake of Stanford. At the meeting, Quake explained how he and his colleagues had sequenced his genome last year in a matter of days. That was the easy part, he said. The hard part was analyzing it and interpreting what it meant for Quake’s health. He was referring obliquely to the new paper.

In the paper, Quake, Church, and their colleagues made a close study of Quake’s family (who have suffered from various sorts of heart disease), and then scoured the scientific literature for every mention of the variants they found in Quake’s genome. They considered the risks these variants posed to Quake for various conditions, but they also took into consideration other sorts of complexity. For example, diseases don’t happen in isolation from each other. If you get obese, for example, you increase your risk of type 2 diabetes. The scientists published a marvelous diagram of the diseases they studied in Quake, with the size of each name corresponding to the size of his risk for each.

The geneticist Daniel Macarthur wrote tonight about this new paper on his blog Genetic Future:

…there are the variants that simply can’t be interpreted. This includes virtually everything seen outside protein-coding regions, and the majority of even those variants found inside coding regions. We simply don’t understand the biology of most genes well enough yet to be able to predict with confidence whether a novel variant will have a major impact on how that gene operates; and we have an even less complete picture of how genes work together to affect the risk of disease.

Like Lupski said, science is hard.

I was wiped out by the end of the morning session. I thought we did a pretty good job, although I still felt ambivalent. I scarfed some lunch and then happily settled into the audience for the afternoon. Most of the talks I heard dealt not with humans but with microbes. The genome of a microbe like E. coli is about a thousandth the size of a human genome. As a result, microbiologists can sequence genomes like mad without busting their budgets. Ian Lipkin of Columbia has hunted for the causes of new outbreaks, such as colony collapse disorder in bees, by fishing out new kinds of microbial DNA from sick hosts. Boom, boom, boom, one slide after another documented the discovery of yet another pathogen. The benefits of DNA sequencing were blindingly obvious in Lipkin’s talk.

But even microbes turn out to have fantastic genomic complexity. There may not be a lot of genes in each microbe, but together they can hold a staggering amount of genetic diversity. Rob Knight of the University of Colorado spoke about the surveys he and his colleagues have made of the human microbiome. He described some of the work I’ve blogged about here on the Loom, along with other results. He described, for example, how children become coated with the bacteria that live in their mother’s birth canal as they are born. Women who have a caesarian section give their children the bacteria living on their own skin. Knight is investigating whether the birth canal germs provide any special protection to children. Different people develop different menageries of microbes as they get older, and their experiences–from gaining weight to taking antibiotics–can shift the ecosystem inside their bodies. There’s much left to discover about the thousands of species that share our bodies with us, but Knight raised the prospect of a different kind of personalized medicine: using genomics to survey the microbes in our bodies and then manipulating them for our own benefit.

Then again, maybe you shouldn’t trust me on this score. Everyone knows I’m in the microbial tank.

The day ended with a talk by Anne West, the 17-year-old daughter of John West. The Times of London recently broke the story of how the Wests became the first healthy family to get their genome sequenced. I expected warm and fuzzy blather about what her genome meant to her, but instead, she delivered a hard-core talk that would have fit right into a genetics conference. She analyzed one of her genes involved in blood clotting and determined that she had a few harmless mutations from her mother and one harmful one from her father. Facing an audience full of past and future Nobel-prize winners, biotech barons, and other intimidating grown-ups, she remained impressively poised and calm.

The audience was rightly impressed. One scientist joked that she should drop out of 11th grade and get a job–finishing school would be a waste of her time. But I also had to remind myself of the hothouse atmosphere in which she had done this work, and in which she was delivering her results. Her father had spent upwards of $200,000 on the family’s genomes, according to the Times. This was not your standard science fair project. And as West spoke, I thought about the kids from a local public high school who had come for the morning session. When Krulwich and I asked the audience for questions, a girl stood up and asked how she could get her mother to have their family’s genomes sequenced, when her mother wasn’t even sure what a gene is. Two girls: two very different experiences with genomes. It’s not all about the DNA.

[PS--Thanks to all the Twitterers who acted as a note-taking collective. Their assembled chronicle is here.]

Ed Yong, thankfully, is all over a new study on how the microbes in the guts Japanese people acquired genes from ocean germs to digest sushi. It’s yet another example of the mind-blowing science emerging from the study of our microbiome–the trillions of non-human organisms that share our body with us. For more on the microbiome, listen to my recent podcast with microbiomist (I just made that up, but it feels so right) Rob Knight.

I’d have blogged on this too, but I’m busy with something in the works for tomorrow. Stay tuned.

Most of life on Earth is a mystery to us. The bulk of biomass on the planet is made up of microbes. By some estimates, there may be 150 million species of bacteria, but scientists have only formally named a few thousand of them. One of the big causes of this ignorance is that scientists don’t know how to raise microbe colonies. If you scoop up some dirt and stick it under a microscope, you’ll see lots of different microbes living happily there. If you mash up all the DNA in that mud and read its sequence, you’ll discover an astonishing diversity of genes belonging to those microbes–thousands in a single spoon of soil. But now try to rear those microbes in a lab. When scientists try, they generally fail. A tiny fraction of one percent of microbe species will grow under ordinary conditions in Petri dish.

This staggering difficulty is the reason why E. coli and a few other species became the laboratory darlings of biologists during the 1900s. As I write in Microcosm, E. coli will happily explode in a flask full of broth. As a result, a lot of what we know about life we know from E. coli. Certainly a lot of those lessons hold true for any species–genes encoded in DNA, DNA used to produce RNA and proteins, a genetic code, and so on. But there are a lot of microbes that are very unlike E. coli. Even in our gut, for example, E. coli is just a minor player in an ecosystem made up of hundreds or thousands of species. Yet we know relatively little about its neighbors.

One reason for the trouble we have in raising microbes is that the environment we like is not the environment a lot of them like. If you are feeding on minerals in boiling water at the bottom of the ocean, it’s possible that you might find life in a luke-warm flask in an oxygen-rich atmosphere at sea-level air pressure unbearable–perhaps even toxic.

But the physical surroundings of microbes can’t account for all the trouble they pose for would-be microbial zoo-keepers. If you scoop up some wet sand from a pleasant beach, you will still be hard-pressed to get more than a few species to grow in the lab.

To coax bacteria to grow, microbiologists have been upgrading their Petri dishes. They have been building cages that mimic the natural habitat of the bacteria, and in some cases taking their chambers out of the lab and putting them in the environments where the bacteria live.

These semi-wild chambers have brought scientists more success, and they’ve also helped scientists figure out why the microbes are so hard to grow in the first place. Along with the right physical conditions, microbes need to live alongside the right microbes.

In the new issue of Chemistry and Biology, a team of scientists–led by Anthony D’Onofrio, a post-doc in the laboratory of Kim Lewis at Northeastern University, and Jason Crawford in the lab of Jon Clardy at Harvard–report a striking success in cultivating bacteria that were previously impossible to cultivate. They made their discovery while studying some bacteria that live on a beach near Boston. Some of the bacteria, while unable to grow on their own in a Petri dish, grew if they were near certain other species. Perhaps, the scientists speculated, the hard-to-grow bacteria depended on something the other species made.

The scientists tested different molecules made by bacteria to see if any of them were fostering the growth. They eventually figured out that the responsible molecule was something known as a siderophore. Some species of bacteria make siderophores as a way to get their minimal daily required does of iron. Iron is essential for the growth of cells, but in many environments free iron is in short supply. So bacteria make iron-trapping molecules–siderophores–and release them through special channels. The siderophores drift around, and sometimes manage to snag iron atoms. They fold up around the iron, assuming a shape that allows them to slip through other channels back into the bacteria. Once inside, they open up again and set their iron free.

It turns out that a lot of species on the beaches around Boston–and presumably in a lot of other places in the world–don’t make their own siderophores. Instead, they rely on other species to produce siderophores, and once those molecules swallow up the iron, the bacteria that don’t make siderophores snatch them up. The scientists found that with different kinds of siderophores made by different species of bacteria, they could suddenly get a lot of microbes to grow.

Discoveries like these are exciting both in a practical and intellectual way. We’ve already harvested lots of valuable molecules from microbes, such as antibiotics and gene-copying enzymes. If scientists can raise lots of new species of microbes, they may be able to find new molecules. But the result is fascinating in itself. Apparently, a lot of microbial species depend on the kindness of strangers. And apparently, there are bacteria out there that are churning out siderophores despite the fact that other species are slurping up the iron they forage. If that was all there was to the story, this would not be a situation that could last long. The cheaters would thrive by skipping the effort of making siderophores, and eventually there wouldn’t be enough honest bacteria left to keep all the microbes supplied with their iron. It’s likely, instead, that the cheaters are not cheaters at all, but rather have services of their own to offer the microbial community.

And so the reason that we know so little about life on Earth may be that we have yet to figure out the complicated social life of microbes.