Erika Check Hayden is a journalist at Nature and educator in San Francisco. Her work has taken her to wild and beautiful places, but focuses most of the time on the inner terrain of the human body. You can find her online at erikacheck.com and twitter.com/Erika_Check.
This piece was originally published at The Last Word on Nothing.
A few years ago, Eric Klavins found himself starting at the ceiling of his room in the Athenaeum, a private lodging on the grounds of the California Institute of Technology, in the middle of the night. Unable to sleep, Klavins was instead pondering a question that had been posed to him earlier that day at a meeting.
Klavins, a robotics researcher, was funded by grants from the U.S. Air Force and the Defense Advanced Research Projects Agency (DARPA) on robot self-organization: making many simple robots work together to assemble themselves into a shape or structure. While working on the grants, Klavins would routinely be called into meetings to discuss his work with various defense officials, and it was at one of these meetings that a Defense Department researcher had posed his question. “He said, ‘Do you think you could figure out how something that has been broken up into lots of little pieces could be reassembled so we could figure out what it was?’” he recalls.
Klavins spent hours thinking about how one could actually do it. Then, he realized, he had no idea why one would even want to—and hadn’t asked that question at all during all the years he worked with Defense Department funding. He suddenly felt uncomfortable about that. “It bothered me that someone would spend their time studying how things get blown up and working to make things get blown up better,” Klavins says. Not long after, he decided to steer away from defense funding and towards applications in biology and medical research that are part of the realm of synthetic biology, the field of science that tries to turn biology into more of an engineering discipline.
But if Klavins thought that the change would help him escape the moral dilemmas that used to keep him up in the middle of the night, he was wrong. The U.S. Department of Defense has emerged as one of the major funders of synthetic biology; last fall, for instance, DARPA accepted proposals for a highly coveted set of grants in a new program, Living Foundries, that aims to “enable the rapid development of previously unattainable technologies and products, leveraging biology to solve challenges associated with production of new materials, novel capabilities, fuel and medicines.”
Earlier this week, food columnist Ari LeVaux set off a storm of media reaction with a piece with this premise: tiny plant RNAs, recently discovered to survive digestion and alter host gene expression, are a major reason why genetically modified foods should be considered dangerous. For anyone familiar with the paper he referred to, or with molecular biology in general, the article was full of conflation and sloppy logic, and even as it became the most-emailed story on TheAtlantic.com, where it was published, biology bloggers and science writers were pointing out its significant flaws. To his credit, LeVaux revised the article to fix many (though not all) of the errors concerning genetics; the new version appeared yesterday at AlterNet and today replaced his original piece at The Atlantic.
So what did LeVaux get so wrong, and, once all of the wheat was sorted from the chaff, was there anything to what he was trying to say?
At the heart of the fracas is LeVaux’s claim that a class of molecules called miRNA is a reason to fear GMOs specifically, more than any other food plant or animal. miRNA, which is short for microRNA, is a class of molecules that perform various tasks in plants and animals. They were first discovered about twenty years ago, in nematode worms, and they regulate gene expression by binding the messenger RNA involved in translating a gene into a protein. The messenger RNA carries the “message” of the DNA’s sequence to a group of enzymes that translate it into the amino acid sequence of a protein. But if a miRNA binds to a messenger RNA, the message is destroyed, and the protein is never made. Thus, miRNA can be a powerful tool for preventing the expression of genes. In fact, that is what’s made it such an important lab tool in recent years: it allows researchers to knock down the expression of genes without physically removing them from an organism’s genome.
In the paper that LeVaux pegged his article on, Nanjing University researchers found that miRNAs usually seen in rice were circulating in the blood of humans, and that mice fed rice had the miRNA in their blood as well. That particular miRNA, in its native context, regulates plant development. When the researchers added it to human cells, it appeared to bind to the messenger RNA of a gene involved in removing cholesterol from the blood. Previous papers had found that plants have plenty of miRNA floating around in them [pdf] (as does just about everything we eat, since plants and animals make them by the thousands), but having them show up whole and unmolested in blood, apparently after digestion, was a new and very intriguing discovery.
Malcolm MacIver is a bioengineer at Northwestern University who studies the neural and biomechanical basis of animal intelligence. He also consults for sci-fi films (e.g., Tron Legacy), and was the science advisor for the TV show Caprica.
A few years ago, the world was aflame with fears about the virulent H5N1 avian flu, which infected several hundred people around the world and killed about 300 of them. The virus never acquired the ability to move between people, so it never became the pandemic we feared it might be. But recently virologists have discovered a way to mutate the bird flu virus that makes it more easily transmitted. The results were about to be published in Science and Nature when the U.S. government requested that the scientists and the journal withhold details of the method to make the virus. The journals have agreed to this request. Because the information being withheld is useful to many other scientists, access to the redacted paragraphs will be provided to researchers who pass a vetting process currently being established.
As a scientist, the idea of having any scientific work withheld is one that does not sit well. But then, I work mostly on “basic science,” which is science-speak for “unlikely to matter to anyone in the foreseeable future.” But in one area of work, my lab is developing new propulsion techniques for high-agility underwater robots and sensors that use weak electric fields to “see” in complete darkness or muddy water. This work, like a lot of engineering research, has the potential to be used in machines that harm people. I reassure myself of the morality of my efforts by the length of the chain of causation from my lab to such a device, which doesn’t seem much shorter than the chain for colleagues making better steels or more powerful engines. But having ruminated about my possible involvement with an Empire of Dark Knowledge, here’s my two cents about how to balance the right of free speech and academic freedom with dangerous consequences.
Consider the following thought experiment: suppose there really is a Big Red Button to launch the nukes, one in the U.S., and one in Russia, each currently restricted to their respective heads of government. Launching the nukes will surely result in the devastation of humanity. I’m running for president, and as part of my techno-libertarian ideology, I believe that “technology wants to be free” and I decide to put my money where my slogan is by providing every household in the U.S. with their very own Big Red Button (any resemblance to a real presidential candidate is purely accidental).
If you think this is a good idea, the rest of this post is unlikely to be of interest. But, if you agree that this is an extraordinarily bad idea, then let’s continue.
Sex, a biological function of reproduction, should be simple. We need to perpetuate the species, we have sex, babies are born, we raise them , they have sex, repeat. Simple, however, is one thing sex most certainly is not. And it’s only getting more complex by the day.
For those who are fans of human exceptionalism, it might be worth considering that the trait which differentiates us from all other animals is that we over-complicate everything. Sex, and its various accoutrements of sexual orientation, gender identity, gender expression, libido, and even how many partners one may have, contains a multitude.
Recently some psychologists have said that pedophilia is a sexual orientation, the erotic predilection that drives people like former Penn State football coach Jerry Sandusky to do what he allegedly did. This idea came to twitter and incited a minor firestorm over whether “sexual orientation” should really be applied to pedophilia. Nature editor Noah Gray used the term in a neutral sense, as in, “an attraction to a specific category of individuals”; io9′s Charlie Jane Anders and Boing Boing blogger Xeni Jardin pointed out the queer community’s long campaign to define sexual orientation only as an ethically acceptable preference for any category of consenting adults. Given that willful troglodytes like Rick Santorum regularly conflate homosexuality with pedophilia and zoophilia, you can see where the frustration around loose use of the term might arise.
Santorum aside, how should we classify pedophilia if not a “sexual orientation?” Why should that term include should one unchosen, inborn form of sexual attraction, but exclude another unchosen, inborn form of sexual attraction?
While we may have ready answers for these questions now, technological and social changes on the horizon will once again challenge our definitions and beliefs about sex. We can imagine a time when we have artificial intelligence (to at least some degree), or super-intelligent animals, or maybe we’ll even become a spacefaring species and encounter other alien intelligences. Without a doubt, people will start discovering that they are primarily attracted to something that isn’t the good ol’ Homo sapiens. Sex and sexuality will increase in complexity by powers of ten. If some person is attracted to a sexy cyborg, or a genetically enhanced dolphin, how will we know if it is ethical to act upon those desires?
by Richard Wrangham, as told to Discover’s Veronique Greenwood. Wrangham is the chair of biological anthropology at Harvard University, where he studies the cultural similarities between humans and chimpanzees—including our unique tendencies to form murderous alliances and engage in recreational sexual activity. He is the author of Catching Fire: How Cooking Made Us Human.
When I was studying the feeding behavior of wild chimpanzees in the early 1970s, I tried surviving on chimpanzee foods for a day at a time. I learned that nothing that chimpanzees ate (at Gombe, in Tanzania, at least) was so poisonous that it would make you ill, but nothing was so palatable that one could easily fill one’s stomach. Having eaten nothing but chimpanzee foods all day, I fell upon regular cooked food in the evenings with relief and delight.
About 25 years later, it occurred to me that my experience in Gombe of being unable to thrive on wild foods likely reflected a general problem for humans that was somehow overcome at some point, possibly through the development of cooking. (Various of our ancestors would have eaten more roots and meat than chimpanzees do, but I had plenty of experience of seeing chimpanzees working very hard to chew their way through tough raw meat—and had even myself tried chewing monkeys killed and discarded by chimpanzees.) In 1999, I published a paper [pdf] with colleagues that argued that the advent of cooking would have marked a turning point in how much energy our ancestors were able to reap from food.
To my surprise, some of the peer commentaries were dismissive of the idea that cooked food provides more energy than raw. The amazing fact is that no experiments had been published directly testing the effects of cooking on net energy gained. It was remarkable, given the abiding interest in calories, that there was a pronounced lack of studies of the effects of cooking on energy gain, even though there were thousands of studies on the effects of cooking on vitamin concentration, and a fair number on its effects on the physical properties of food such as tenderness. But more than a decade later, thanks particularly to the work of Rachel Carmody, a grad student in my lab, we now have a series of experiments that provide a solid base of evidence showing that the skeptics were wrong.
Whether we are talking about plants or meat, eating cooked food provides more calories than eating the same food raw. And that means that the calorie counts we’ve grown so used to consulting are routinely wrong. Read More
One of the strangest aspects of our understanding of evolutionary biology is the tendency to conflate a sprawling protean dynamic into a sliver of a phenomenon. Most prominently, evolution is often reduced to a process driven by natural selection, with an emphasis on the natural. When people think of populations evolving they imagine them being buffeted by inclement weather, meteors, or smooth geological shifts. These are all natural, physical phenomena, and they all apply potential selection pressures. But this is not the same as evolution; it’s just one part. A more subtle aspect of evolution is that much of the selection is due to competition between living organisms, not their relationship to exterior environmental conditions.
The question of what drives evolution is a longstanding one. Stephen Jay Gould famously emphasized of the role of randomness, while Richard Dawkins and others prioritize the shaping power of natural selection. More finely still, there is the distinction between those which emphasize competition across the species versus within species. And then there are the physical, non-biological forces.
Evolution as selection. Evolution as drift. Evolution as selection due to competition between individuals of the same species. Evolution as selection due to competition between individuals of different species. And so forth. There are numerous models, theories, and conjectures about what’s the prime engine of evolution. The evolutionary biologist Richard Lewontin famously observed that in the 20th century population geneticists constructed massively powerful analytic machines, but had very little data which they could throw into those machines. And so it is with theories of evolution. Until now.
Over the past 10 years in the domain of human genetics and evolution there has been a swell of information due to genomics. In many ways humans are now the “trial run” for our understanding of evolutionary process. Using theoretical models and vague inferences from difficult-to-interpret signals, our confidence in the assertions about the importance of any given dynamic have always been shaky at best. But now with genomics, researchers are testing the data against the models.
A recent paper is a case in point of the methodology. Using 500,000 markers, ~50 populations, and ~1,500 people, the authors tested a range of factors against their genomic data. The method is conceptually simple, though the technical details are rather abstruse. The ~1,500 individuals are from all around the globe, so the authors could construct a model where the markers varied as a function of space. As expected, most of the genetic variation across populations was predicted by the variation across space, which correlates with population demographic history; those populations adjacent to each other are likely to have common recent ancestors. But the authors also had some other variables in their system which varied as a function of space in a less gradual fashion: climate, diet, and pathogen loads. The key is to look for those genetic markers and populations where the expectation of differences being driven as a function of geography do not hold. Neighbors should be genetically like, but what if they’re not? Once you find a particular variant you can then see how it varies with the factors listed above.
Every few years it seems that the British biologist Steve Jones declares the death of evolution by natural selection in the human species. The logic here is simple even to a schoolboy: evolution requires variation in fitness, and with declining risk by death during our reproductive years humans have abolished the power of selection. But this confuses the symptom for the disease. Death is simply one way that natural selection can occur. Michelle Duggar has 19 children. The average American woman has around two by the end of her reproductive years. It doesn’t take a math whiz to figure out that Michelle Duggar is more “fit” in the evolutionary sense than the average bear. Even without high rates of death, some people have more children than other people, and if those people who have more children than those who do not are different from each other in inherited traits, evolution must occur. Q.E.D.
But you probably shouldn’t be convinced by logic alone. Science requires theory, experiment, and observation. (If you’re talking humans, you can remove the second from the list of possibilities: there are certain unavoidable ethical obstacles to experimenting on human evolution—plus we take far too long to reproduce.) But humans sometimes have something which bacteria can not boast: pedigrees! Not all humans, of course. Like most of the world’s population I don’t have much of a pedigree beyond my great-grandparents’ generation. But luckily for biologists, the Catholic Church has long taken a great interest in life events such as baptism, marriage, and death, and recorded this info parish by parish. With these basic variables, demographers can infer the the rough life histories of many local populations over the centuries. In many European nations, these databases can go more than 10 generations back. And some aspects of human evolution are revealed by these records.
What aspects am I talking about? Reproduction itself. Not only is variation in fitness one of the primary ways by which evolution occurs, but it is also a trait upon which evolution operates! How else are there rabbits which breed like…rabbits, and pandas…which don’t. There is often variation within species for the odds of multiple births, age at first reproduction, and lifespan, depending upon the differences in selection pressures over a population. And that seems to be exactly what occurs in human beings. There is interesting evidence for evolution of reproductive patterns from populations as diverse African pygmies and Finns, but more recently some researchers have been plumbing the depths of the records of the Roman Catholic Church in Quebec, and they’ve come back with gold.
Consider two pandemics: the white-nose syndrome now devastating North American bats and the Black Death that killed a third or more of Europeans in the 14th century. Lethality aside, they may not seem to have much in common. But recent studies suggest they both offer important lessons about understanding that the deadliness of disease organisms is very much a product of the circumstances in which they appear.
Two weeks ago in Nature, a multi-institutional team of U.S. Geological Survey scientists presented conclusive evidence the parasitic fungus that lends white-nose syndrome its name is indeed the cause of the mysterious bat epidemic. The illness came to light in New York in 2006, when cave explorers started finding thousands of little brown bats (and later, other species) dead together in the caves where they spent the winter months, their bodies covered with a white fungus, Geomyces destructans. It has since spread throughout the northeastern U.S., where bat populations have declined on average by 73 percent—which may make it one of the most rapid declines in wildlife populations ever observed. Worse, white-nose syndrome is still on the move, with documented cases in four Canadian provinces and states as far south and west as Tennessee, Missouri, and Oklahoma.
This post was originally published at Ed Yong’s Discover blog, Not Exactly Rocket Science.
Two people are dancing a waltz, and it is not going well. One is tall and the other short; one is graceful, the other flat-footed; and both are stepping to completely different rhythms. The result is chaos, and the dance falls apart. Their situation mirrors a problem faced by all complex life on Earth. Whether we’re animal or plant, fungus or alga, we all need two very different partners to dance in step with one another. A mismatch can be disastrous.
Virtually all organisms with complex cells—better known as eukaryotes—have at least two separate genomes. The main one sits in the central nucleus. There’s also a smaller one in tiny bean-shaped structures called mitochondria, little batteries that provide the cell with energy. Both sets of genes must work together. Neither functions properly without the other.
Mitochondria came from a free-living bacterium that was engulfed by a larger cell a few billion years ago. The two eventually became one. Their fateful partnership revolutionised life on this planet, giving it a surge of power that allowed it to become complex and big (see here for the full story). But the alliance between mitochondria and their host cells is a delicate one.
Both genomes evolve in very different ways. Mitochondrial genes are only passed down from mother to child, whereas the nuclear genome is a fusion of both mum’s and dad’s genes. This means that mitochondria genes evolve much faster than nuclear ones—around 10 to 30 times faster in animals and up to a hundred thousand times faster in some fungi. These dance partners are naturally drawn to different rhythms.
This is a big and underappreciated problem because the nuclear and mitochondrial genomes cannot afford to clash. In a new paper, Nick Lane, a biochemist at University College London, argues that some of the most fundamental aspects of eukaryotic life are driven by the need to keep these two genomes dancing in time. The pressure to maintain this “mitonuclear match” influences why species stay separate, why we typically have two sexes, how many offspring we produce, and how we age.