Here are a few numbers about DNA–some big ones, and then some very small ones.

The human genome contains about 3.2 billion base pairs. Last year, scientists at the University of Leceister printed the sequence out in 130 massive reference-book-sized volumes for a museum exhibit. From start to finish, they would take nearly a century to read.

A typical gene is made up of a few thousand bases. The human genome contains about 21,000 genes that encode proteins. There are other genes in the human genome that encode molecules known as RNA, but how many of those RNA molecules actually do anything useful in the cell is a matter of intense debate. A lot of the human genome is made of neither protein- or RNA-coding genes. Much (maybe most) of it is made up of dead genes and parasite-like stretches of DNA that do little more than making copies of themselves.

As I wrote recently in the New York Times, 3.2 billion base pairs and 21,000 genes are not essential requirements for something to stay alive. E. coli is doing very well, thank you, with a genome about 4.6 million base pairs. That’s .14% the size of our genome. Depending on the strain, the microbe has around 4100 protein-genes. That’s about a fifth the number of protein-coding genes that we carry. The high ratio of genes to genome size in E. coli is the result of its stripped-down, efficient genetics. Mutations that chop out non-functional DNA spread a lot faster in microbes than in animals.

E. coli, in turn, has proven to be positively gargantuan, genetically speaking, compared to some other species. As scientists explore more of the microbial world, they find species with smaller genomes. In my column for the Times, I wrote about the record-holding tiny genome, belonging to a microbe called Tremblaya. Its genome is a mere 139,000 base pairs. That’s .004% the size of our genome. You could print the entire sequence in a single slim paperback you could slip in your pocket. And in that sleek genome are just 120 protein-coding genes–.6% of our own collection of protein-coding genes.

Whenever I report on such record-breakers, I try to stress that they are only breaking records at that moment. Tremblaya has the smallest genome known. Or, I should now say, it had the smallest genome known last month.

This month in the journal Genome Biology and Evolution, Gordon Bennett and Nancy Moran describe a new record holder, called Nasuia deltocephalinicola. It has a genome of just 112,000 base pairs. Imagine taking that slim novella and ripping off the last chapter. Ironically, Nasuia packs in more genes into its DNA than Tremblaya–137 protein-coding genes, Bennett and Moran estimate.

What’s really striking about all these current and former record-holders for small genomes is that they all live in a single exotic ecological niche. Without exception, they can be found inside plant-feeding insects. Tremblaya lives in mealy bugs, for example, while Nasuia lives in a leafhopper (Macrosteles quadrilineatus).

Inside those hosts, these microbes carry out chemical reactions on the food that the insects eat. The insects feed on sap and other fluids from plants, which contains few nutrients. But the bacteria can use the compounds floating in the fluid to build amino acids, which the insects can then assemble into proteins.

Leafhoppers, cicadas, sharpshooters, and other related insect species carry related versions of the same stripped-down bacteria. By drawing their evolutionary trees, Bennett and Moran have found that the insects got into a symbiotic relationship with the microbes over 260 million years ago. I’ve reproduced their tree below for those who want some gory details. The blue lines show Nasuia and related lineages of microbes. The insects also acquired another species of bacteria, known as Sulcia. Together, these two microbes split the work for millions of years. (In some insects, fungi also jumped into the mix.)

The ancestors of Nasuia started out as free-living microbes that had genomes on par with E. coli. But once they got inside a host, they were able to lose DNA without paying a price. The insects gave them a stable home, building special organs to shelter them, and they even pass down the bacteria to their offspring. The bacteria cast aside many genes that might otherwise seem essential, such as a number of genes involved in generating energy. All they needed to do was continue to provide a service, by synthesizing some amino acids.

Nasuia holds the record now, but probably not for long. There are many other species of insects left to investigate. Moran had John McCutcheon of the University of Montana have done some back-of-the-envelope calculations to figure out how much smaller the genomes of those symbionts can get. All known insect symbionts share 82 genes in common. It’s possible those genes are absolutely required to survive as a symbiont. But a symbiont also needs to provide a benefit to its host, or its host will likely get rid of it. It takes at least 11 genes to synthesize a single amino acid. Those 93 genes, McCutcheon and Moran estimate, could fit in a genome as small as 70,000 base pairs.

It’s funny that these bacteria allow us to probe one of the most basic questions about life: how simple life can get and yet still qualify as being alive? While those who make fun of science for a living may consider such research a waste of time, studying these stripped-down organisms is also about as practical as science can get. The leafhoppers that house Nasuia, for example, are a nightmare for farmers, causing damage to a wide range of vegetables by spreading fungi and bacteria. Yet they would be helpless if not for their exquisitely simple lodgers. If we can understand how they survive with such tiny genomes, we may be able to stop them from enabling their hosts.

From Bennett and Moran 2013
From Bennett and Moran 2013

The Stanford biologist Stephen Palumbi wrote an excellent book some years ago called The Evolution Explosion, in which he argued that humans have become a powerful force in the evolution of life. We’ve altered the whole planet, so that now many species are traveling on new evolutionary trajectories. (For more, here’s a review of the book I wrote for the New York Times Book Review.)

Over the years since Palumbi’s book came out, scientists have documented more examples of our effect. This week, I was intrigued to come across a new study that we may be even altering the brains of animals. It’s the subject of my new Matter column for the New York Times. It’s only a preliminary study, of course, but it does raise some fascinating questions about the mental challenges animals now face as they navigate a human-dominated world. Check it out.

When Charles Darwin developed his theory of evolution, he resigned himself to only seeing its effects. Evolution happened so slowly, he was convinced, that we couldn’t see life changing from one generation to the next by a mechanism such as natural selection. So he found other ways to amass evidence for evolution.

He pointed out, for instance, that natural selection was a logical–even inescapable–fact of life. Individuals varied in their traits. Some of those variations influenced how many offspring they had. And those traits could also be passed down to offspring. Under such conditions, natural selection just happens.

Darwin also looked back over the history of life and showed how powerfully evolution could explain its large-scale patterns. He couldn’t account for every jot and tittle over the past four billion years, of course. But he could, for example, account for how groups of species shared sets of traits: because they descended from a common ancestor that lived millions of years ago.

Starting in the mid-1900s, however, evolutionary biologists  began documenting measurable evolution over the course of years, not millennia. As chronicled by Jonathan Weiner in The Beak of the Finch, for example, Peter and Rosemary Grant have measured changes in the beaks of Darwin’s finches over the past four decades.

Microbes–which breed much faster than animals and acquire mutations at a faster rate–are also opening new lines of research into evolution. Scientists like Richard Lenski and Paul Turner are tracking the evolution of bacteria and viruses over a matter of weeks, or even days.

This week in my “Matter” column for the New York Times, I took a look at a new study on experimental evolution. Bacteria living in Petri dishes evolved extra tails, which allowed them to swim faster and take over their populations. The experiment is fascinating in many ways–from its potential applications to medicine to what it says about the predictability of evolution. Plus, it comes with cool videos.

While the response to my column has been generally enthusiastic (thanks), I have gotten some negative comments that echo an old refrain I often hear when I write about experimental evolution. Basically: they’re still bacteria.

 

Here’s a related chain of tweets…

 

 

Opponents of evolution often like to decree what evolution really is. That way, when scientists study evolution, they can declare, “That’s not evolution.”

Nevathir, for example, claims that that what happened in this experiment is just “pattern formation,” which apparently refers to how dogs give birth to puppies that have different color patterns. (That’s not actually called pattern formation, but I have to guess here.)

Puppies get different color patterns because (among other reasons) they inherit different combinations of genes from their parents. The experiments I wrote about this week are not “pattern formation” in this sense of the phrase. They started with genetically identical bacteria, which divided, producing identical clones except when new mutations arose. Those mutations were then passed down to their descendants. Mutations to one gene in particular led to the emergence of “hyperswarmers.” Hyperswarmers were genetically programmed to make more tails, which allowed them to swim faster than their ancestors. And they quickly drove slower bacteria extinct as they came to dominate the population.

That is evolution–evolution in under a week, in fact.

V. Hugo asks what new traits were created. Apparently acquiring a number of new tails is not a new trait, in the same way that a mutation in people can lead to the development of an extra finger on the hand. And apparently changes can only be called evolution if they involved the evolution of a new trait.

It’s very hard for me to see how evolving from a single tail to up to half a dozen tails–all of which work together rather than getting tangled up with each other–is not a new trait. But even if we go along with V. Hugo this far, his sort of argument still fails, because it’s not an argument at all. He’s just creating a personal definition of evolution in order to scoff at scientific research.ÂThe origin of new traits is part of evolution, but so is the spread of beneficial mutations due to natural selection.

I suspect that Nevathir and V. Hugo aren’t satisfied with this experiment because it isn’t a large-scale episodes of evolution–the split between species, for example, or the origin of an eye or a hand. (I’m guessing here, but it’s a guess educated on many previous such comments.) Large-scale episodes take time, typically stretching across thousands or millions of years. The scientists who study bacteria over the course of a few weeks don’t expect to witness such transformations. Instead, they are finding that they can dissect the mechanisms of evolution. They can even document the emergence of new genes, as mutations accidentally duplicate stretches of DNA, which can then begin to take on new functions.

And then there’s the “They’re-still-bacteria” remark. I hear variations of this refrain many times, which makes me assume that it gives opponents of evolution great comfort. Bacteria are one “kind” of life form, and since these experiments don’t show them evolving into another “kind”–like a dog–then they reveal nothing.

Such a remark isn’t just wrong-headed about evolution, though. It reveals a misunderstanding of bacteria. Bacteria originated about 3.5 billion years ago and have been diversifying into many different forms ever since. Some bacteria float in the ocean, turning sunlight into carbon. Others breathe iron. Others make squid glow. Watching bacteria evolve in a Petri dish helps us to understand not just evolution in general, but bacteria in all their particulars.

Since the mid-1900s, medical researchers have dreamed of fixing genetic disorders by supplying people with working versions of genes. By the late 1990s, that dream–known as gene therapy–seemed very, very close. Scientists were developing engineered viruses that would infect patients with DNA that would allow their bodies to make the proteins they needed to survive.

But then, in 1999, a young man who had volunteered for a trial died. The whole field of gene therapy went into a tailspin. Only in recent years has it recovered.

I’ve written a story for Wired about that turnaround, focusing on the career of the scientist who oversaw that fateful 1999 trial, James Wilson. For the past fourteen years Wilson been hunting for better viruses for gene therapy, and his viruses are now involved in some of the most promising research for treating diseases ranging from hemophilia to blindness. To find out more about Wilson and gene therapy, check out “The Fall and Rise of Gene Therapy.”

Let me just say at the outset that this post is about the baculum. Some of you may not want to read about the bone found in the penises of many mammal species. I want to give you a chance to head off for tamer blogs. But you might want to stick around. There’s some real science below–and some evolution in action.

Last week in the New York Times I wrote about the evolution of monogamy (here and here). The occasion for the articles were two new studies in which scientists analyzed hundreds or thousands of species of mammals, tracing the evolution of monogamy and other social arrangements. This big-picture approach to evolution can yield some important insights, but the finer details are hard to make out.

If you look at us humans (monogamy, polygamy, and assorted other stuff) versus chimpanzees (monogamy is for losers!), you’re only looking at the tips of two deep branches. Chimpanzees may be our closest living relatives, but our common ancestor with them lived about seven million years ago. After the two lineages split from that ancestor, they’ve been evolving in different directions ever since. We can make some inferences about what that evolution was like based on ourselves, chimpanzees, and other living mammal species. But this kind of research doesn’t give us a visceral sense of how the sexual habits of mammals evolve from generation to generation.

That’s why it was so interesting to come across a new study from Leigh W. Simmons and Renée Firman at the University of Western Australia. They’ve been able to observe sexual evolution of mammals unfold in their laboratory. Last week’s studies were like a satellite view of the continents. Here, we’re down on the ground.

How males and females live with one another depends on the conditions in which their species lives. If a single male can mate with lots of females, for example, he will end up with a lot of offspring. But if the females are spread out too far, he may not be able to guard them all from other males who want to mate with them too. In such cases, natural selection may favor males that prefer to stick with just one female.

In species where males compete with each other a lot for females, evolution may produce new pieces of anatomy. Some males evolve extravagant horns to fight off rivals. Even their genital anatomy can change. This is likely to happen when females mate with many males. The males fight against each other even during sex. Some male insects, for example, using spiny genitals to scrub out their competitors’ sperm.

Evolutionary biologists hypothesized that these extravagant sexual organs were the result of an evolutionary race between males. They found support for this idea when they compared individual males to each other. It turned out that the males that had the most offspring tended to have the spiniest penises.

More recently, researchers have started to watch these organs evolve. In 2011, for example, Swiss scientists reported a study they carried out on seed beetles, which have spines on their genitals for scrubbing away rival sperm.

The Swiss scientists isolated each male with just one female. In that arrangement, the males had no competition for mates. The researchers then let the beetles mate for 21 generations. The spines on the male’s genitals got measurably smaller. That’s just what scientists had predicted based on evolutionary theory. Without any competition from other males, there was no advantage to spiny penises.

Simmons has documented a lot of the evidence for this evolution of male genitals in insects, and now he and Firman have turned their attention to mammals. To be more precise, they’ve turned their attention to the baculum–a bone that they call “one of the most puzzling enigmas of mammal morphology.”

The baculum is long in some species and stubby in others; it can be straight or hooked, barbed or shaped like Neptune’s trident. In a few species, like our own, it’s just missing altogether.

Scientists have developed several possible explanations for its existence. Some have suggested that by making the penis rigid, the baculum lets a male deliver more sperm into a female. Those extra sperm may outnumber those of rival males. Others have suggested that the baculum helps the sperm travel further towards an egg. Still others have proposed that it stimulates the female, triggering ovulation.

All three hypotheses have something in common: the baculum evolves thank to its ability to translate mating into fathering. In June, some British researchers published a study that supported that idea. They studied house mice, a species in which females mate with many males each time they’re ovulating. The scientists found that male mice with a wider baculum had more mouse pups than other males.

Simmons and Firman took this research to the next logical step. They reasoned that this difference between male mice should drive the evolution of the baculum. To find out, they ran an experiment similar to the one run by the Swiss scientists. They created two groups of mice: promiscuous maters and monogamous maters.

The promiscuous females got to mate with three males in each cycle. The monogamous ones only got to mate with one. They bred the mice for 27 generations and then took a look at their bacula. As with the seed beetles, the baculum evolved. It became thicker in the promiscuous group and thinner in the monogamous one. For the first time, scientists had observed the baculum evolving.

The experiment still doesn’t solve the mystery of what the baculum for, but Simmons and Firman do have an idea about that–at least for mice. They think that the baculum helps male mice stimulate the female reproductive tract. That stimulation may make it more likely that the male fertilizes the female’s eggs, or raises the odds that a fertilized egg successfully implants itself in her uterus.

If the baculum is indeed driven by sexual selection in mammals, the question naturally arises: where’s ours? “Why human males lack a baculum remains enigmatic,” Paula Stackley, a biologist at the University of Liverpool, wrote last December in Current Biology.

Among primates, monogamous species tend to have much smaller bacula than species where males compete for mating. So it wouldn’t be crazy to assume that the shift towards monogamy in our ancestors made the human baculum disappear altogether (except for a very, very few scary cases).

Things aren’s so simple as all that, however. Chimpanzees, our closest relatives, are far from monogamous. You’d think they had a huge baculum, but it’s only about the size of a grain of rice–about five times smaller than a baboon’s baculum. In fact, all the great apes have tiny bacula. For some mysterious reason, this mysterious bone has been vanishing in our ancestors for some ten million years or more. While the bacula can evolve in a matter of weeks in a scientific experiment, its evolution can stretch out across deep time, as well.