Aphids, those sap-sucking foes of gardeners, come in a variety of colours. We usually think of them as green, but pea aphids sometimes wear a fetching red ensemble. That may not strike you as anything special; after all, lots of animals are red. But the aphid’s colour is unique in a couple of extraordinary ways.

The colour comes from pigments called carotenoids. Animals use them for all sorts of purposes; they act as antioxidants, and they contribute to red, orange and yellow colours. But the pea aphid is one of only a few known species (all aphids) that manufacture their own carotenoids; everyone else gets theirs from their food. But it’s the source of the pea aphid’s ability that’s truly remarkable – it stole the skill from fungi. By integrating fungal genes into its own genomes, it gained a superpower that almost all other animals lack.

These sorts of “horizontal gene transfers” go on all the time in bacteria, but they’re supposedly a rarity among more complex creatures like animals and plants. And yet, scientists have recently documented several examples of such transfers. Rotifers smuggle genes from fungi, bacteria and plants. “Space Invader” genes have jumped across animals as diverse as lizards and bushbabies. One bacterium, Wolbachia, has even inserted its entire genome into that of a fruit fly. And parasites can transfer their genes to humans.

In most of these cases, it’s unclear whether the imported genes are actually doing anything useful. But the story of the pea aphid, told by Nancy Moran and Tyler Jarvik, is very different. The colour of a pea aphid determines the predators that target it. Ladybirds (one of their major enemies) prefer to attack red aphids on green plants but parasitic wasps are more likely to lay their eggs in green aphids, to fatal effect. Colour clearly matters to an aphid, so here is a clear example of a transferred gene shaping an obvious trait in its new host and in doing so, shaping its evolution.

Moran and Jarvik knew that both red and green pea aphids have carotenoids, but their source was a mystery. These pigments dissolve easily in fat but not water, and they’re unlikely to be found in the plant sap that the aphids suck. Aphids carry beneficial bacteria but none of their genomes carry any traces of the genes required for creating carotenoids. And aphids that are cured of their hitchhikers don’t lose their colour. So where do the carotenoids come from?

Fortunately, Moran and Jarvik knew what to look for, since all organisms that make carotenoids, including plants, fungi and bacteria, do so with a common set of genes and enzymes. They also knew where to look, for the genome of the pea aphid had been recently sequenced. Their search yielded seven genes that are clearly involved in producing carotenoids. But to their surprise, none of this septet matched any gene in any other animal genome. Instead, their closest relatives are found in fungi.

Moran and Jarvik think that the original donor was a species of fungus that either infected the ancestors of today’s pea aphids, or formed an alliance with them. Either way, we know that this mystery donor transferred at least two genes to the insects, which have since duplicated into the current seven. And we know that the relocation happened before the pea aphid diverged from the related peach-potato aphid, which has the same genes.

Today, the genes explain the two hues of the pea aphid. The green aphids have carotenoids that are yellow in colour. The red ones do too, but their palette is bolstered by two bright red carotenoids that the green aphids lack. The greens can’t make these extra pigments because one of their seven fungal genes is missing a small sizeable chunk. This broken gene means that the green aphids can’t complete a chemical reaction that converts one of the yellow carotenoids into the two red ones.

The pea aphid’s story tells us that genetic swaps between complex species like fungi and animals are possible, although probably still rare. Before now, scientists did actually try to search the pea aphid genome before for genes transferred from other species. But they only looked for genes of bacterial origin; no one considered that the donors might be fungi, so the carotenoid-making genes were never found.

When Moran and Jarvik searched for other fungal genes, they didn’t find any, demonstrating that such swaps are the exception rather than the rule. But what fascinating exceptions – and the growing number of full animal genomes will surely help us to discover more.

Reference: Science http://dx.doi.org/10.1126/science.1187113

Image: by Charles Hedgcock

More on aphids:

• Virus and bacteria team up to save aphid from parasitic wasp
• Aphids defend themselves with chemical bombs
• Are red autumn leaves a warning sign to insects?
• The suicide plasterers – aphids that repair their homes with their own bodily fluids
• Aphids hide from parasitic wasps among the corpses of their peers

More on horizontal gene transfer:

• Gut bacteria in Japanese people borrowed sushi-digesting genes from ocean bacteria
• Dormant viruses can hide in our DNA and be passed from parent to child
• Attack of the killer tomato fungus driven by mobile weapons package
• Genes from Chagas parasite can transfer to humans and be passed on to children

Last week, NASA presented the first images and videos from its latest and greatest eye on the Sun: the Solar Dynamics Observatory.

SDO has been in the works for a long, long time, and I’ve been anxiously awaiting data from it for years… so of course I was away from my computer when the images were released. Still, it was worth a few extra days to see something as back-of-the-neck-hair-raising as this:

Holy Haleakala! Click to emprominate.

As if on cue, just days after SDO’s Atmospheric Imaging Assembly (AIA) was switched on, the Sun threw an epic fit, blasting out an arcing prominence perfectly positioned for us to see. A prominence is a loop of gas that erupts from the surface of the Sun. This gas follows the Sun’s magnetic field lines; complicated interplay between the energy stored in the field lines versus their tension causes them to leap up from the Sun, anchored in two spots that represent where the north and south poles of the lines punch through the Sun’s surface. A prominence might have as much as a hundred billion tons of matter in it, and can be hundreds of thousands of kilometers across.

To give you an idea of this, here’s a video made from images from AIA:

Kaboom! Interestingly, the gas isn’t as hot as you might think, and can be cooler than the surface of the Sun. When we see a prominence edge-on, silhouetted against the surface of the Sun, it actually appears dark! When that happens, we call it a filament.

I’ve been a big fan of the Solar and Heliospheric Observatory (SOHO) for a long time, and SDO is like the Son of SOHO. It has technology that is more current, and has very high resolution cameras. SDO can take spectra of the Sun to look in detail at its composition, temperature, motion, and magnetic strength. It can also measure the seismology of the surface of the Sun, the way waves travel across it and make it pulse; this tells us about the interior of the Sun that is otherwise totally invisible. Combining all this data together yields a vast amount of knowledge waiting to be learned about our nearest star.

It also produces stunning full-Sun imagery:

This image is amazing; it shows very hot helium and iron ranging in temperature from 60,000 Kelvin (100,000+° F) to well over a million Kelvins (1.8 million degrees F)! You can see the big prominence to the left, as well as several others around the disk. All the twisting and writhing on the surface is due to the bubbling convection of hot material from the Sun’s interior rising to the surface coupled with the fiercely complex solar magnetic field. The physics involved is incredibly complex, but with SDO’s help scientists will soon have a much firmer grasp on what’s going on.

Of course, they’ll also have a pile of new mysteries to ponder as well. The Sun is the closest star to the Earth, and closer than most planets. We know a lot about it, but there’s so much left to understand: what’s the root cause of the 5.5 year long solar magnetic cycle? How is that tied to Earth’s climate? What effect do sunspots have on the Sun and Earth? How exactly does the Sun influence space weather; the flood of subatomic particles streaming from the solar surface and interacting with our own magnetic field, affecting satellites and even our power grid?

Science is like a tapestry with no edge, and with holes located here and there in the fabric. We can fill those holes ever more, and explore the edges, pushing them back with each new discovery. Along with many other observatories like it, SDO is our loom that helps us create and follow that weave.

Credit: NASA/SDO/AIA, NASA/GSFC/SDO/AIA

A few months ago I blogged a paper in PLoS Biology which suggested that a common Y chromosomal haplogroup, in fact the most common in Europe and at modal frequency along the Atlantic fringe, is not pre-Neolithic. Rather their analysis of the data implied that the European variants were derived from an Anatolian variant. The implication was that a haplogroup which had previously been diagnostic of “Paleolithicness,” so to speak, of a particular population may in fact be an indication of the proportion of Neolithic Middle Eastern ancestry. The most interesting case were the Basques, who have a high frequency of this haplogroup, and are often conceived of as “ur-Europeans,” Paleolithic descendants of the Cro-Magnons in the most romantic tellings. I was somewhat primed to accept this finding because of confusing results from ancient DNA extraction which implies a lot of turnover in maternal lineages, the mtDNA. My logic being that if the mtDNA exhibited rupture, then the Y lineages should too, as demographic revolutions are more likely to occur among men.

But perhaps not. A new paper in PLoS ONE takes full aim at the paper I blogged above. It is in short a purported refutation of the main finding of the previous paper, and a reinstatement of what had been the orthodoxy (note the citations to previous papers). A Comparison of Y-Chromosome Variation in Sardinia and Anatolia Is More Consistent with Cultural Rather than Demic Diffusion of Agriculture:

Two alternative models have been proposed to explain the spread of agriculture in Europe during the Neolithic period. The demic diffusion model postulates the spreading of farmers from the Middle East along a Southeast to Northeast axis. Conversely, the cultural diffusion model assumes transmission of agricultural techniques without substantial movements of people. Support for the demic model derives largely from the observation of frequency gradients among some genetic variants, in particular haplogroups defined by single nucleotide polymorphisms (SNPs) in the Y-chromosome. A recent network analysis of the R-M269 Y chromosome lineage has purportedly corroborated Neolithic expansion from Anatolia, the site of diffusion of agriculture. However, the data are still controversial and the analyses so far performed are prone to a number of biases. In the present study we show that the addition of a single marker, DYSA7.2, dramatically changes the shape of the R-M269 network into a topology showing a clear Western-Eastern dichotomy not consistent with a radial diffusion of people from the Middle East. We have also assessed other Y-chromosome haplogroups proposed to be markers of the Neolithic diffusion of farmers and compared their intra-lineage variation—defined by short tandem repeats (STRs)—in Anatolia and in Sardinia, the only Western population where these lineages are present at appreciable frequencies and where there is substantial archaeological and genetic evidence of pre-Neolithic human occupation. The data indicate that Sardinia does not contain a subset of the variability present in Anatolia and that the shared variability between these populations is best explained by an earlier, pre-Neolithic dispersal of haplogroups from a common ancestral gene pool. Overall, these results are consistent with the cultural diffusion and do not support the demic model of agriculture diffusion.

Their main trump cards seem to be that they used a denser set of markers, and, they claim they have a more accurate molecular clock. Ergo, in the latter case they produce a better time to the last common ancestor, which is twice as deep as the paper they’re attempting to refute. Someone like Dienekes or Polish Genetics can tackle the controversies in scientific genealogy here (I know Dienekes has a lot of interest in mutational rates which go into the molecular clock for these coalescence times). Rather, I would suggest that usage of Sardinians concerns me for an obvious reason: they’re genetic outliers in Europe. A lot of this has to do with being an island. Islands build up uniqueness because they don’t engage in the normal low level gene flow between adjacent populations because they’re…well, islands. You would know about Sardinia’s position because they’re one of the populations in L. L. Cavalli-Sforza’s HGDP sample and they show up in History & Geography of Human Genes as on the margins of the PCA plots. But here’s a figure from a more recent paper using a much denser market set, constrained to Southern European populations. I labelled some of the main ones so you’d get a sense of why I say Sardinians are outliers:

Over the two largest independent dimensions of genetic variation you can see a distribution from the southeast Mediterranean all the way to the northwest (in fact, the Basques are an Atlantic group). The Sardinians are out of the primary axis, and that’s why I say they’re an outlier. A few other European groups, like the Icelanders and Sami exhibit this tendency. As I suggested above I think the fact that the Sardinians are on an isolated island relatively far from the European and Africa mainland means that they’ll “random walk” in genetic variation space toward an outlier status naturally, just as the Icelanders have since the year 1000. So though I grant the authors their rationale for using the Sardinians as a reference against the Anatolian source population, the fact that we know that they’re peculiar in their variation in total genome content makes me wary of drawing too many inferences from their relationships to other groups where they are seen as representative of a larger set.

Citation: Morelli L, Contu D, Santoni F, Whalen MB, & Francalacci P (2010). A Comparison of Y-Chromosome Variation in Sardinia and Anatolia Is More Consistent with Cultural Rather than Demic Diffusion of Agriculture PLoS ONE : 10.1371/journal.pone.0010419

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.]

NASA/JPL Cassini with Huygens probe intact

Have you been keeping up with Cassini?  Today (April 27th Pacific and April 28th UTC) it’s scheduled to make a flyby of Enceladus, passing as close as 60 miles above the surface of the moon.  According to the mission counter, the closest point in the flyby will be at about 7pm CDT, April 27th – United States.

NASA/JPL artist's conception of Enceladus flyby

Cassini will fly through the water-rich plumes over the moon’s south polar region.  In addition, Cassini scientists will be conducting gravity studies on this flyby which will help determine what lies beneath the ice crust on the surface of Enceladus.

NASA/JPL South Pole of Enceladus

All the data we have up to this point indicates there is an ocean of liquid water under the ice crust.  Because of this, Enceladus looks very likely to be a source of life.

NASA/JPL Close-up of South Pole region of Enceladus

I would really, REALLY like to get a sample from those plumes under my microscope.

Can I look? Oh-please-oh-please-oh-please!

I have to say, this made me smile. And even laugh.

True enough, Hubble got me. I can’t even complain that it’s the Bubble Nebula, not galaxy. Even I’m not that picky.

Some vaccine news I missed in the past few days…

1) A pertussis outbreak in California has already killed two infants. This event resonates with what happened in Australia a year ago; vaccination rates are low, and the victims are too young to be vaccinated themselves. With herd immunities compromised, the littlest and most defenseless reap the effects. This is not necessarily caused by the antivaxxers, but it’s worth noting.

2) There is apparently a small outbreak of polio in Tajikistan. Vaccinations are critical, but so is sanitation.

3) PBS airs a documentary called "The Vaccine Wars" tonight. It’s about what you think it’s about. Check your local listings.

4) H1N1 is still out there, and still hurting and killing kids.

5) A bunch of kids got pretty sick after vaccinations in Australia. It’s unclear what happened, and officials are investigating it.

6) The good news? At least for Finland, it’s good: 97% of kids there are vaccinated. For everything. Amazing.

Tip o’ the needle to Antti Säämänen, Doug Troy, William Mount, and Greg Stitz.

An observational study of consumer use of fast-food restaurant drive-through lanes: implications for menu labelling policy. "OBJECTIVE: ... The present study was designed to quantify the number of customers who purchase fast food through drive-in windows as a means of informing legislative labelling efforts. DESIGN: This was an observational study. SETTING: The study took place at two McDonald's and Burger King restaurants, and single Dairy Queen, Kentucky Fried Chicken, Taco Bell and Wendy's restaurants. SUBJECTS: The number of customers entering the chain restaurants and purchasing food via the drive-through lane were recorded. A total of 3549 patrons were observed. RESULTS: The percentage of customers who made their purchases at drive-throughs was fifty-seven. The overall average (57 %) is likely a conservative estimate because some fast-food restaurants have late-night hours when only the drive-throughs are open. CONCLUSIONS: Since nearly six in ten customers purchase food via the drive-through lanes, menu labelling legislation should mandate the inclusion of menu labels on drive-through menu boards to maximise the impact of this public health intervention." Photo: flickr/s2art Related content:
Discoblog: NCBI ROFL: Alice Waters would not approve.
Discoblog: NCBI ROFL: Fresh squeezed orange juice odor: a review.
Discoblog: NCBI ROFL: eat me.

It was a big week for experimental military aircraft, with the Air Force’s secretive X-37B space plane and the Navy’s biofuel-powered “Green Hornet” both achieving successful test flights. But the most ambitious—the HTV-2 hypersonic glider under development by the Defense Advanced Research Projects Agency (DARPA)—lost contact with its operators during its run.

Launched from Vandenberg AFB, Calif. on April 22, the unmanned HTV-2 was planned to cross the Pacific and impact the ocean north of Kwajalein Atoll in the first of two flights to demonstrate technology for a prompt global strike weapon [Aviation Week]. It successfully achieved separation from its booster rocket high in the atmosphere; however, nine minutes into the test the glider lost communication. Now the military is studying the test flight telemetry to figure out where the HTV-2 would have crashed down.

Thursday’s mission was the first of two planned in the HTV-2 program, which uses Minotaur 4 boosters developed by Orbital Sciences Corp. from decommissioned Peacekeeper intercontinental ballistic missiles. The U.S. military is trying to develop technology to respond to threats around the globe at speeds of Mach 20 or greater, according to DARPA [AP]. DARPA is being fairly tight-lipped about possible uses for the HTV-2, but it’s not hard to see why the military would be excited about an aircraft that travels about 13,000 miles per hour and can strike on the other side of the world with “little or no advanced warning,” as the agency says.

Program manager Paul Erbland says the key to HTV-2 flying at such speed and height is its carbon shell, which is capable of withstanding extreme heat and pressure. It doesn’t burn off material to get rid of heat. The vehicle is designed to fly at a low angle of attack relative to other hypersonic vehicles. “Shuttle and similar vehicles fly at roughly 40°; HTV-2 is substantially below that,” he said [Aviation Week]. As for the communications failure, DARPA has some time to address the problem before the craft’s second planned test flight next March.

Related Content:
80beats: Will the Pentagon Build the Jetsons’ Flying Car?
80beats: Highway to the Green Zone? Navy To Test a Supersonic Biofuel Jet
80beats: DARPA Wants a Biofuel Jet, While Germany Works on a Hydrogen Plane
80beats: DARPA’s Kooky $40,000 Scavenger Hunt

Image: DARPA

When it comes to the relationship between bees and African elephants, size does not matter. The massive pachyderms are terrified of bees, which can painfully sting elephants around their eyes and inside their trunks. Baby elephants are the most vulnerable to bee stings, as their skin isn’t thick enough to ward off the insects. And researchers have now found that the elephants have developed a special strategy to help them avoid these bees that scare the bejesus out of them.

When an elephant takes note of a swarm of bees, it emits a distinct rumbling call. This bee alarm, which the scientists termed a “bee rumble,” helps draw the herd’s attention to the bees and allows them to run off unharmed, the researchers write in the journal PloS ONE. What’s more, they respond to an audio recording of the bee rumble as if it were the real thing, giving farmers a tool they could potentially use to fend off unwanted elephants.

This is the first time that an alarm call for a specific threat has been identified in elephants. Lead researcher Lucy King of the University of Oxford believes that such calls may be an “emotional response” to a threat and a way to co-ordinate group movements. Ms King explained: “We discovered elephants not only flee from the buzzing sound, but make a unique rumbling call, as well as shaking their heads” [BBC]. The head-shaking looked like an attempt to fend off or dislodge the bees that the elephants assumed were buzzing around, King says.

For the study, King and her team played the recordings of the bee rumble vocalization to 10 elephant families. Six of the families immediately got up and fled, despite the fact that they had neither seen nor heard any bees. When the scientists tweaked the vocalization a bit to remove a key acoustical feature found in bee rumbles, the elephants stayed put. The researchers suggest that elephants may also have warning calls to alert their fellows to humans and lions—much like Diana monkeys in West Africa can call out a leopard alarm or eagle alarm, depending on which predator they spot [ScienceNOW].

King hopes that recordings of the bee rumble can be used by farmers to chase away elephants and keep them from trampling fields. As agriculture expands in Africa, elephants have been squeezed into tighter habitats–causing them to stray across fields and damage crops. “Farmers will do anything to keep their crops and families safe from damage, and unfortunately records of shootings, spearings, and poisonings of elephants are on the increase,” Ms King wrote on the University of Oxford’s website [BBC]. King hopes that playing back the bee rumble around fields could serve as a low-tech, humane deterrent to elephants, who will then be sent packing back into the woods.

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80beats: Memories of Hard Times Might Help Elephants Survive Global Warming

Image: Lucy King/Oxford University

A handful of fun things that shouldn’t pass unremarked:

• Natalie Wolchover, an aspiring science writer, has started a fun blog called Facto Diem. For those of you who didn’t attend Catholic school, that’s Latin for “Fact of the Day.” (Or a close enough facsimile.) I didn’t even know there were that many facts in the world!
• In the more venerable sections of the blogosphere, Chad Orzel is running a poll concerning the most amazing application of lasers. Considering that “death ray” is not among the options, it’s a pretty good list.
• We should also link to Scientia Pro Publica #27, over at Melliferax. (Clearly Latin is the lingua franca of the science blogosphere.) Most of the posts involve living things in some way or another, but they should nevertheless be of interest to those of us with more inorganic inclinations.

For the tiny flatworm, regeneration of missing body parts is a piece of cake. Someone chopped its head off? No problem! It grows a brand new one in about seven days, complete with a spanking new brain with all the right circuits and connections. (As for the chopped-off head, it just grows a new body.) This amazing ability of the flatworm to regrow a missing head and to produce a brain on demand has now been traced back to a key gene, researchers report in a PloS Genetics study. The identification of the gene is exciting news for scientists who wonder if humans, too, can one day learn to regenerate missing body parts. The Register reports that the discovery of the "smed-prep" gene unlocks the mechanisms by which the hard-to-kill Planarian flatworms grow new muscle, gut, and brain cells:
Even more importantly, it seems that the information contained in smed-prep also makes the new cells appear in the right place and organize themselves into working structures – as opposed to nonfunctional blobs of protoplasm.
Lead researcher Aziz Aboobaker describes the worm's regenerative superpowers to the BBC:
"One of the reasons they can do this is because they're chock-full of stem cells. We estimate that at ...

Heather Steingruebl is a BABloggee. She contacted me and told me some chilling news: her daughter Elise was recently diagnosed with leukemia. She’s being treated, and I know we all hope things go well for her.

But in the meantime, this makes Elise susceptible to many preventable diseases. We need people to get vaccinated! As Heather says,

Vaccinate. Elise and thousands of kids like her are counting on not dying from things like measles and whooping cough while they fight cancer. Unless it’s a specific health risk to you or your child, just vaccinate. Please.

She also implores people to get on the bone marrow donation registry. Search around online for information on how to do this. I plan on doing this myself.

My heart goes out to her and her family, as it does to anyone affected by this awful illness. I’m going to find out what booster shots I need, because I take this issue very seriously. I hope you do too.

Scientists have long suspected that a link exists between mood and chocolate, as studies (done primarily with women) have suggested that eating a chocolate bar temporarily banished the blues. Now a study has brought new complexity to the issue with its finding that depressed people consume larger amounts of chocolate. But researchers are no closer to figuring out which factor is the cause and which is the effect: Do glum people reach for a Hershey bar to lift their spirits, or is the chocolate actually bringing them down?

For this study, researchers at the University of California studied 931 men and women who weren’t on antidepressants and quizzed them on their chocolate-chomping habits. Then, using a standard screening survey, they assessed the volunteers for symptoms of depression. The scientists found that those who were the most blue consumed the most chocolate.

This held true for both the men and the women; people who were depressed ate an average of 8.4 servings of chocolate per month, compared with 5.4 servings among those who were not depressed [Reuters]. Those who scored highest on the mood tests, indicating possible major depression, consumed an average of 11.8 servings per month [Los Angeles Times]. The findings led the research team to conclude in the Archives of Internal Medicine that “depressed mood was significantly related to higher chocolate consumption.”

While the study established a link between chocolate eating and depression, the researchers could not pin down how the two things are related. The authors suggest that depression might stimulate chocolate cravings, and that people might reach for a candy bar to self-medicate; chocolate prompts the release of certain chemicals in the brain, such as dopamine, that produce feelings of pleasure [Los Angeles Times]. But it’s also possible chocolate only provides a short-term lift, and that over time, it contributes to depression. Yet another possibility is that a separate physiological mechanism, like stress, is responsible for both depression and an appetite for chocolate. With this cloud of uncertainty hovering over the candy isle, chocoholics will be eagerly awaiting further studies.

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80beats: Are Women’s Brains Hard-Wired to Have Trouble Resisting Temptation?
80beats: For Obese Women, a Milkshake Brings Less Pleasure to the Brain

Image: iStockphoto

Flight and fluid dynamics scientist Adrian Thomas of the The Oxford Animal Flight Group made this motion study of a tethered desert locust. As it turns out, the gorgeous look of this video is dictated by the constraints of shooting insects and smoke currents. The black and white makes it easier to shoot, by providing more flexibility with two additional F-stops, and reducing the elements to their most basic parts. Thomas used high-speed video, shooting at 1000 frames per second in order to catch the 20-per-second wing beats of the locust, blasting it all with five kilowatts of light to bring out the smoke. Using another neat trick, the smoke is created by heating baby oil. The desert locust is a good subject because it tolerates the heat and light and is likely to behave normally in these conditions.

These careful studies of insect flight dynamics have yielded significant results. Thomas: “The major obstacle to small micro-air-vehicles is power efficiency. The power density of current battery technologies is not sufficient to allow current flapping micro-air-vehicles to fly for long enough periods to be effective. The careful design of insect wings is one of the features that allows insects smaller than current micro-air-vehicles to achieve migratory flights taking many days and crossing continents.”

Video and still image courtesy Adrian Thomas, Animal Flight Group, Oxford University

Four decades ago, the Soviet Union put a reflector on the moon able to bounce laser signals back to the Earth. There was just one problem: They lost it.

But now the marooned reflector has been found, thanks to the determined hunting of University of California, San Diego researchers. NASA’s Lunar Reconnaissance Orbiter, in orbit around the moon, photographed the landing area where the USSR’s Luna 17 mission dropped off the missing reflector, Lunokhod 1, in 1970. The photos turned up a faint reflective dot, and the team thought that was it.

With an idea now where to point their own laser, the researchers received a stronger signal back from Lunokhod 1 than they ever had in years of studying its sister craft, Lunokhod 2. “The best signal we’ve seen from Lunokhod 2 in several years of effort is 750 return photons, but we got about 2,000 photons from Lunokhod 1 on our first try,” said Murphy. “It’s got a lot to say after almost 40 years of silence” [UPI].

After landing near the Mare Imbrium, Lunokhod 1 stayed in touch with Soviet ground controllers for no less than 11 months, prowling the moon even as the US astronauts of Apollo 14 and 15 were driving about elsewhere in their manned moon buggies. However the robot crawler eventually ceased communications, and the project was officially terminated on October 4, 1971 [The Register]. The Soviet scientists lost the location of the reflector, and because it doesn’t reflect enough light from the sun for us to see it from Earth, they never found it again. Firing the laser to look for a signal only works if you know the reflector’s general location, and thus wasn’t possible until the LRO spotted Lunokhod 1 this year.

The American team had used Lunokhod 2 along with three reflectors left behind by Apollo missions to keeps tabs on our natural satellite and track its position and orbit as it ever-so-slowly moves away from us. And the researchers say that the re-discovered Russian reflector is particularly useful for studying the moon’s liquid core and testing ideas about gravity [Scientific American].

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Bad Astronomy: Apollo Landing Sites Imaged by LRO!
Bad Astronomy: LRO First Light Images of the Moon!

Image: NASA

If you thought a cow was good only for its milk and meat, then we'd have you know that somewhere between Oklahoma City and Fort Worth, Texas, there is an Amtrak train chugging along on moo-power. Amtrak is currently running its Heartland Flyer train on a mix of traditional diesel fuel and biodiesel produced from cow products, in an experiment that Amtrak argues could make railroads more eco-friendly. The Heartland Flyer uses about 100,000 gallons of diesel fuel each year to move 84,000 people. For this one-year test run, Amtrak will replace 20 percent of that fuel with biodiesel, produced from tallow from Texas cows. The fat from the cattle, which is normally used to make animal feed and soap, will now instead help power a train. According to Fast Company:
Amtrak says that the cow tallow (read: rendered fat from cattle) fuel reduces hydrocarbon and carbon monoxide emissions by 10%, cuts down on particulates by 15%, and reduces sulfates by 20% compared to standard diesel.
But if the idea of whizzing across the heartland in a cow-powered train makes you uneasy, then you're not alone. The animal rights organization PETA isn't too hot on the idea either, with PETA spokesman Bruce Friedrich telling Fast ...

If you thought the toxic bubbling lakes of asphalt DISCOVER covered on Friday were impressive, you ought to see what’s under the sea just off the California coast: giant volcanoes made from the same stuff we use to pave our roads.

Lead author David Valentine and his colleagues first found these asphalt volcanoes in 2007 when they sent submersible robots to explore peculiar formations 700 feet below the surface. Now, in a study in Nature Geoscience, the team has published its findings and its images of the extinct volcanoes. Valentine says the formations are six stories high, and spread out farther than a football field. “If I could convert all the asphalt in the largest volcano to gasoline, it would be enough to fuel my Honda Civic for about half a billion miles” [National Geographic], he says.

Valentine first used the aquatic robot Alvin to explore the volcanoes and take samples; the robot’s operators describe the experience as like driving a flat road and suddenly seeing an enormous mountain rise up in front of you. The researchers then deployed the autonomous bot Sentry. “When you ‘fly’ Sentry over the seafloor, you can see all of the cracking of the asphalt and flow features,” Valentine said. “All the textures are visible of a once-flowing liquid that has solidified in place” [LiveScience].

These huge mounds formed 31,000 to 44,000 years ago as petroleum oozed out from the seafloor, the team’s chemical analysis suggests. Over time, the petroleum mixed with sand and debris and hardened into domes. There are also depressions around the largest volcanoes that used to be massive vents of methane, the scientists say. They argue that those vents could have contributed to a spike in the level of methane in the ocean about 35,000 years ago, which researchers knew about before this find.

If indeed the volcanoes once blasted huge amounts of methane into the sea, then the plethora of methane-eating bacteria, combined with the oil reaching the surface and creating slicks, could have created a dead zone for most life. But that was then. Now, with the methane emissions reduced to a few tiny vents, oceanographer Ian MacDonald says that could be turned on its head: These unusual formations could present an opportunity for marine organisms to thrive. “I think it’s really cool that there’s this other process that we didn’t really know about before that, at least in some places, is making pretty extensive hard bottoms for animals to colonize” [National Geographic].

And while the nation’s oil and ocean focus is set on the Deepwater Horizon disaster in the Gulf of Mexico, coauthor Chris Reddy said in a statement that the asphalt volcanoes are a reminder not to forget the natural part of the equation. “The volcanoes underscore a little-known fact: Half the oil that enters the coastal environment is from natural oil seeps like the ones off the coast of California.”

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Images: Jack Cook, WHOI; George Foulsham, UCSB

A few weeks ago I reviewed a paper on the the genetics of the Cape Coloured population. Within it there was a refrence to another paper, Deconstructing Jaco: genetic heritage of an Afrikaner. The title refers to the author himself. It was an analysis of his own pedigree going back to the 17th century, along with his mtDNA, his father’s mtDNA, and his Y lineage. The genetics is a bit thin, but the pedigree information is of Scandinavian quality from what I can tell. Praised the records of the Reformed Church!

The author’s utilizes an inversion of the typical method whereby a survey of a population may give some insight into individuals within that population. Rather, he leverages the thorough church records of his Afrikaner community, and his local roots, to paint a picture of his own ancestry. Then he compares the results to those of the community as a whole. Though an N of 1 certainly has limits it seems that the author concludes that he is relatively representative because some of the statistics that emerge out of pedigree analysis seem to fall in line with what genealogists working with the whole community have found. Additionally, it is clearly that he has deep roots within the historic Afrikaner nation, so assuming random mating and little population substructure, inferences from his pedigree may have some general utility.

Afrikaners apparently have some peculiarities genetically which has made them of some interest to scientists. It turns out that they seem to exhibit high frequencies of classical Mendelian diseases, a hallmark of inbreeding or population bottlenecks. This aligns well with the thesis that Afrikaners are the descendants of a small group of founders who arrived in the 17th century and entered into a long phase of demographic expansion, which culminated with their long Trek into the veld to escape English domination as well as perpetuate their practice of slavery (James Michner’s The Covenant is a fictionalization of this). As I have observed before the primacy of the “first settler” seems to loom large in the minds of demographers.

J. M. Greef, the author of the above paper, seems to refute this simple story in his own genealogy, though not the core aspect of the importance of the first founders. First the abstract:

It is often assumed that Afrikaners stem from a small number of Dutch immigrants. As a result they should be genetically homogeneous, show founder effects and be rather inbred. By disentangling my own South African pedigree, that is on average 12 generations deep, I try to quantify the genetic heritage of an Afrikaner. As much as 6% of my genes have been contributed by slaves from Africa, Madagascar and India, and a woman from China. This figure compares well to other genetic and genealogical estimates. Seventy three percent of my lineages coalesce into common founders, and I am related in excess of 10 times to 20 founder ancestors (30 times to Willem Schalk van der Merwe). Significant founder effects are thus possible. The overrepresentation of certain founder ancestors is in part explained by the fact that they had more children. This is remarkable given that they lived more than 300 years (or 12 generations) ago. DECONSTRUCT, a new program for pedigree analysis, identified 125 common ancestors in my pedigree. However, these common ancestors are so distant from myself, paths of between 16 and 25 steps in length, that my inbreeding coefficient is not unusually high (f approximately 0.0019).

Inbreeding coefficient is the probability that one’s two alleles are identical by descent. That is, they come from the same individual. For example, in the case of Elisabeth Fritzl her children have many genes where the alleles are identical by descent because half of her own genes are from her father, some many of his alleles will come back to reside within the same individual as part of a diploid pair. J. M. Greef notes that his inbreeding coefficient is about twice as high as is the norm for the typical European. Europe is a region of relatively low consanguinity, so this is a stringent reference. In some populations the inbreeding coefficient can be as high as 0.01. In short, he’s not too inbred.

That being said, the data within his pedigree do seem to show disproportionate contribution by some ancestors. This makes sense for two primary reasons. First, some component of reproductive variance is random (often modeled as a poisson distribution). Second, some component of reproductive variance is due to innate fitness (e.g., the Genghis Khan Y haplotype may be a case of this). Equality of contribution just isn’t in the cards.

Figure 2 shows the distribution of relationships within the pedigree:

Panel a illustrates that one individual is an ancestor of the author 30 times over! Many individuals are ancestors only once. Panel b shows relatedness, and again, some individuals are much closer to the author than others, with a skewed distribution. Panel c shows the number of generations between the ancestor and the author. The median number is well above ten generations, so the author has deep roots in South Africa. Finally, panel d shows the number of steps between his parents for any given ancestor. Because the author’s parents are both Afrikaners they share many common ancestors, but the steps between seem relatively large, and confirms that the author is not particularly inbred (if the parents were first cousins naturally there would be much shorter steps to common ancestors). It is clear disproportionate amount of J. M. Greef’s genes come from early settlers. This makes sense insofar as demographic expansion was likely front loaded, with later settlers having less of a chance to make an impact on an already large population.

The following table shows the contribution by various European and non-European groups to the author’s ancestry, as well as estimates for the total Afrikaner population in earlier studies on the right.

Note one point: only a minority of the ancestry of the author and Afrikaners are ethnically Dutch. This is important, because it shows how culture can spread and overwhelm ancestry. The Dutch imposed their language upon the French Huguenots, and their religion upon the Germans (who I presume were mostly Lutheran if they were from northern Germany, though a minority were Reformed or Catholic surely). Obviously the Reformed Calvinist religion and Afrikaans language both have a unique stamp in South Africa, but the connection of the Afrikaners to the Netherlands remained profound rather late in history. The Prime Minister of South Africa from 1958-1966 was born in the Netherlands. And yet another fact hard to deny is that the Huguenot French component seems to have persevered to a greater extent culturally than the German. The last Afrikaner President was named F. W. de Klerk, his surname being a form of Le Clerc. Another prominent South African head of state was Daniel Francois Malan. The author observes:

It is not clear if my higher estimate of French contribution is because of a systematic mistake in Heese’s (1970) estimate, or if it is because of a quirkiness in my own ancestry. It seemed to be the case that when a lineage hit the French Huguenots it stayed in this group. It will be interesting to compare the degree of inbreeding of the early generations of Huguenots to the other early immigrants. In the light of the calculations of Heyer et al. (2005) there is an interesting possibility that the cultural inheritance of fitness may have led to a systematic bias in Afrikaners, since Huguenots tended to be more educated and trained than German emigrants who tended to be soldiers. We are currently investigating this hypothesis.

There is a joke that the Baltic possessions of the Swedish monarchy were conquered with Finnish soldiers. Similarly, the Dutch overseas colonial possessions were staffed, especially at a lower level, by the rural male population surplus of northern Germany. A great many of these, likely the vast majority, never returned home and died abroad. These men contributed greatly to the census size of the Afrikaner population during much of its history, but it seems plausible that their fitness was far lower than the established Dutch and Huguenot groups because they lacked the resources and capital to flourish in a world which was much closer to the Malthusian edge than today. Many people don’t leave descendants, and it seems plausible that these Germans were fated not to do so to a far greater extent than the Dutch and Huguenots whom they were employed to protect and serve. Because of the genetic closeness of the north German and Dutch populations (in reality, Dutch are really simply another group of north Germans who transformed their regional identity into a national one for various reasons) I doubt that more thorough genetic testing will resolve this, rather, more pedigree analysis needs to be done on other individuals. But it’s an insight into the fact that social parameters have often been crucial to fitness in the human past.

As for the non-white component, the author’s results match those of previous researchers. He confirmed the likely probability of these results by the fact that his father carries mtDNA group M, which is most diverse in India. And in fact his father’s maternal lineage does trace back to a woman who was likely an Indian slave (slave women had particular surnames indicating their origin). My previous posts on the Coloureds highlighted the large Asiatic component to their ancestry, and it looks like previous researchers ignored this and focused on the Khoisan and Bantu. They also attempted to calculate ancestry based on classical markers which were found in African populations, and are present in low frequencies in Afrikaners, but that might ignore Asian signature markers (additionally, I assume that there was some natural selection for G6PD alleles). A survey of the total genomes of Afrikaners should be able to resolve the details of their ancestry, but it seems that the Afrikaners are far more colored than white Americans, by a factor of 5, but far less than white Latin Americans like Argentineans, probably by a factor of 5.

Finally, the author was also able to assess whether his ancestors exhibited a trade between quantity and quality in terms of their optimal number of offspring. In other words, did those who favored an extreme r or K selected strategy suffer vis-a-vis those who produced a more moderate number of offspring, not too low, and not too high? The author did not find any evidence of a tradeoff, and an optimal fitness. He was careful not to generalize too much, especially in light of the fact that Dutch colonial South Africa was an atypical society in many ways. I assume that living on the frontier means not having to say you’re sorry if you breed too much or too little.

Citation: Greeff, J. (2007). Deconstructing Jaco: Genetic Heritage of an Afrikaner Annals of Human Genetics, 71 (5), 674-688 DOI: 10.1111/j.1469-1809.2007.00363.x

Over the past three years, I've blogged nearly every day at least once. Today I'm going on vacation... without a laptop! For the month of May, The Intersection will return to its roots as Chris Mooney flies solo once again, but he'll be in excellent company: I've lined up a series of terrific guest bloggers that will appear throughout the month! Readers can look forward to diverse contributions from several terrific writers and scientists and I hope you'll welcome them here and participate in comments. By the time I return, I'll be 30 times round that spectacular star of ours. So see you in June!