Carl Zimmer's Blog, page 4
July 14, 2017
Genomes, microbiomes, and brains: Who are you anyway?
July 6, 2017
Mixing Genes on the Tree of Human Evolution
June 29, 2017
Understanding the Genetics Revolution
June 23, 2017
Heading to Aspen!
September 24, 2015
More Stories, Always More Stories
After a long stretch of quiet here on the Loom, I wanted to let you know what I’ve been up to, and what I’m going to be up to over the next couple years. I’ve got some new projects afoot.
1. Each week I’ve continued to write my “Matter” column for the New York Times, about subjects ranging from vaccines to the Cambrian Explosion. I won’t break down the whole list of recent columns here, but if you ever feel the urge to catch up, you can go to the Matter archive.
2. Two of my books are coming out as second editions. A Planet of Viruses will be out on October 6. It will include updates on Ebola, MERS, and other viruses in the news. Evolution: Making Sense of Life, a college textbook about evolution I co-authored with biologist Doug Emlen, came out in its second edition in July.
3. Assorted other stuff happened this summer: Speaking of viruses, Radiolab podcasted a long talk I had with hosts Jad Abumbrad and Robert Krulwich about their place in life (the viruses, not Jad and Robert). I wrote for the Open Notebook about how to explain science. I was the subject of a profile along with my brother Ben in the New York Observer. And I interviewed writer Steve Silberman for Wired about his book on autism, Neurotribes.
4. I am starting a new book. It will be about heredity, from its baffling past to its increasingly manipulated future. I got the idea in the spring, and over the summer my old friend and editor Stephen Morrow at Dutton (who edited three of my first books) agreed to take it on. It’s been wonderful to start visiting people for my research. But I confess the enormous stack of research books covering my desk daunts me each morning. (No publication date set yet.)
5. I am also starting a new gig. I’m very excited to begin contributing to a new online publication about medicine and the life sciences called Stat, as a national correspondent. Stat was founded by Boston Globe Media and is now led by Rick Berke, who previously worked as executive editor at Politico and assistant managing editor at the New York Times. He has assembled at Stat, which will have its official launch next month. I will be doing a mix of things for them each month (some writing, some other stuff) in which I’ll explore medical research. Details to come. (A note to fellow science writers: I’ll be participating in a panel about Stat’s launch at MIT next month in conjunction with Science Writers 2015. Details about when and where are here.)
—As I continue writing my column each week for the Times, embark on my new book, and gear up for Stat, it’s clear that these three things are going to gobble up pretty much all my free time for at least a year (and probably also my un-free time as well…). So I’ll need to take a break from the Loom until things loosen up again. National Geographic will continue to archive the Loom’s twelve (!!) years’ worth of posts. The science tattoo emporium is going nowhere. Eventually, I’ll be back.
In the meantime, you’re in amazing hands with Brian, Ed, Erika, Maryn, Nadia, and Robert here at Phenomena.
If you’d like to keep posted on stories I publish and other misadventures, please sign up for my email newsletter, Friday’s Elk, which I will continue to send out. (Technical note: over the summer I switched from MailChimp to TinyLetter. I transferred my mailing list, but it’s possible that a few people fell through the cracks. If you didn’t get my first TinyLetter-hosted issue of Friday’s Elk on August 23 and would like to continue receiving it, please sign up at TinyLetter.)
As always, I’m deeply grateful to all of you for reading my stories in whatever form they take, and for joining me on this endless dive into the strange world that science reveals to us.
September 2, 2015
Fighting the Second Skeleton
The skeleton of Harry Eastlack
Fibrodysplasia ossificans progressiva is an incredibly rare disease, striking just one out of every two million people. It’s also an incredibly astonishing disease. A single mutation to a single gene causes muscles to spontaneously turn into new bones. Over time, people with fibrodysplasia ossificans progressiva (FOP for short) grow a second skeleton–one that can cut their lives short.
I wrote about FOP in “The Girl Who Turned to Bone” in the Atlantic in 2013. At the time, FOP served as a microcosm for the struggles of people with rare diseases. (In the United States, almost 30 million people have rare diseases of one kind or another.) Rare diseases have historically attracted little interest from scientists or pharmaceutical companies. Working on common diseases like cancer or diabetes seemed more likely to lead to rewards, both academic and financial. As I wrote in my article, Fred Kaplan of the University of Pennsylvania got a lot of puzzled looks from his colleagues when he decided in the late 1980s to dedicate his career to figuring out FOP. It seemed like professional suicide. And he has certainly traveled a hard road since then. It took many years for him and his colleagues to find the gene behind FOP. And then they spent many more years trying to understand how a mutation to that gene actually leads to the disease. In the meantime, Kaplan has not had any effective treatment to offer his patients with FOP.
I ended my Atlantic story on a hopeful note, observing how rare diseases like FOP were starting to gain more attention–thanks in part to the efforts of patients themselves, as well as new initiatives from the National Institutes of Health. But in the two years since the story came out, things have changed a lot faster than I would have predicted. Rare diseases are attracting a huge amount of attention, which is leading to some potential treatments. One sign of this progress is a study on FOP that’s being published today in the journal Science Translational Medicine. A team of scientists has found a molecule that appears to block the second skeleton.
The gene behind the disease, called ACVR1, encodes a molecule that sits on the surface of cells. There it can grab signaling molecules and relay messages to the interior of the cell. A team of scientists at Regeneron Pharmaceuticals engineered human cells so that they carried the mutation to ACVR1 that is found in people with FOP. Then they hurled a barrage of molecules at the cells, to see if the mutant ACVR1 responded in a peculiar way to any of them. They discovered one that triggered just such an odd response.
The molecule is called activin A. It is released by cells to help with many different tasks in the body, from the development of organs in embryos to healing wounds. The fact that activin A helps heal wounds is especially intriguing when you consider one of the most striking features of FOP: people with the disease often abruptly grow new bones after injuries–even slight ones like bumping into a table corner. Kaplan and other researchers have long wondered if the mutation that causes FOP alters the body’s ability to heal wounds. Instead of causing stem cells to rebuild muscle and other damaged tissue, the body might signal them to become bones. And activin A might carry that faulty signal. In normal cells, it silences ACVR1, but in mutant cells, it excites the receptor.
To test that possibility, the scientists developed mice that carry the FOP-causing mutation. The mice formed new bones in much the same way people with FOP do. The scientists found that if they inserted a sponge soaked in activin A into the mice, the sponge turned to bone.
If they could block activin A, the scientists reasoned, they might be able to stop the chain reaction that creates new bones. In another line of research, Regeneron scientists had developed antibodies that latched onto activin A–and only activin A. When the scientists injected these antibodies into FOP-model mice, they prevented the animals from forming any new bones. Full stop.
The fact that researchers at a company like Regeneron made this discovery is telling. Pharmaceutical companies have increasingly turned their attention to rare diseases in recent years, because, paradoxically, the rare disease market may turn out to be very profitable.
Companies are rolling out drugs with sky-high price tags. Even if they’re used by relatively few people, the companies can make a lot of money. In one demonstration of how times have changed, the rare-disease company called Baxaltra is going to be bought soon for a reported $30 billion. Whether the expensive price for rare-disease drugs are really justified, however, is becoming a matter of intense debate.
Fred Kaplan, who wasn’t involved in the new study, hailed it as a “landmark” in a commentary he wrote with colleagues for the International Fibrodysplasia Ossificans Progressiva Assocation. But there are still many challenges scientists will have to face before activin A can become an effective drug for FOP.
For one thing, researchers have to see if it works as well in people as it does in mice. But because people with FOP are so sensitive to injuries (even a muscle injection can trigger a new bone), regular human trials won’t work. Fortunately, Kaplan and his colleagues have discovered that they can harvest bone-generating stem cells out of baby teeth from children with FOP. So they’re now trying to replicate the activin A studies with these cells.
Setting aside the possible medical potential of this research, it drives home just how mysterious rare diseases can be. FOP might seem like it should be a simple disease to treat. After all, it’s caused by a single mutation to a single gene. But it’s actually fiendishly complex, because it disturbs an intricate web of chemical reactions that our bodies use to grow muscles and bones. The search for a cure for FOP has been going on for over a quarter of a century, and yet no one thought to consider activin A. A normal version of ACVR1 doesn’t relay activin A’s messages. And so no one even guessed that a mutant version would.
“As Alfred Hitchcock demonstrated with clarity,” Kaplan and his colleagues write, “the best way to conceal reality is to hide critical clues in broad daylight.”
[Photo of Harry Eastlack via University of Pennsylvania]
[Update: Corrected the affiliation of the researchers]
June 10, 2015
Of CRISPR and dragons
The good folks of Radiolab and I sat down to talk about the past and future of everyone’s favorite gene-editing tool, CRISPR. Listen here!
June 3, 2015
Please Welcome Robert Krulwich to Phenomena!
Robert Krulwich is a host of the show Radiolab, but he’s also a blogger, having written many posts over the years for National Public Radio. I’m delighted to welcome Robert to Phenomena, which is host to his new blog, “Curiously Krulwich.”
(Full disclosure: I’ve known Robert for a long time. We first met to hunt for autumn leaves in my neighborhood. And we’ve carried on a long-running conversation on a variety of topics such as whether parasites are terrible or awesome. Spoiler alert: they are awesome.)
To celebrate Robert’s arrival, I asked him a few questions about his blogging experiences:
You started out in television, then headed into radio. How did blogs make their way into your creative stream?
Like anything in life, first you hear a strange word, blog, and you wonder “What could that mean?” It sounds like something you’d find on a tugboat. Then, knocking around the web, I bumped into a few, and the ones I bumped into six years ago were gorgeously written, dazzlingly illustrated (bldgblog by Geoff Manaugh, Jason Kottke’s daily roundup at Kottke.org, Information is Beautiful from David McCandless, LoverofBeauty from I don’t know who, he never tells), each one wildly different from the other, yet all of them classy, dangerous, totally new to me, and I thought, how do I get in on this? I have story ideas all the time. I like to draw. I like to write. The fact that NPR (where I was at the time) is a radio network, and isn’t exactly into eyeball products, being more into ears, was no problem. They have a website and they let me launch a science based, sometimes meandering blog, Krulwich Wonders, where I wrote about history, animals, plants, puzzles, math, chemistry, music, art — and found a delightful audience of crabby, over-informed, sometimes charming, sometimes maddening readers who loved telling me how wrong I was or how right I was, while mailing me ideas that kept me going many times a week. It was so much fun. One time I even got a note from astronaut Neil Armstrong when I wondered out loud why he didn’t wander a larger patch of the moon when he visited up there. Here’s why, he barked back, sending me a long, fascinating letter that gave me goosebumps. So how’d I fall into blogging? I fell very, very happily, and when NPR downsized last year and let me go, I felt a little empty inside and wanted a new place to do it. This, I am happy to announce, is the place.
Does blogging feel the same as what you do on RadioLab, or does it feel like a different way to express yourself?
Well, the conversational tone is the same. I want to sound like myself. I don’t want what I do to be too studied, too formal, or too packaged. I want to sound like some guy who sits next to you on a train and turns out to be a good storyteller, and to your surprise (and, I’m hoping, delight) isn’t a bore. That’s how I try to be on the radio. That’s how I’ll try to be here. But, of course, there’s an obvious difference. On the radio (or the podcast) I’m playing with sound, and the thrill is to invent into your ear (which I do with my “genius” pal, Jad). On my blog, I’m playing with your eye. Every post I do is intentionally visual; it features something to look at; sometimes a video, sometimes a series of drawings, sometimes a photo, sometimes something I devise with friends that’s interactive and let’s you play with an idea. The important thing is that both Radiolab and the blog are designed to spill something you didn’t know into your head as intelligibly and as joyously and as carefully as I know how. That’s the goal; to make you learn something you didn’t think you needed or cared to know, but whoosh! Now you know it. That’s what I like to do.
You work in lots of artwork into your blog posts. What’s the process behind that? Do the artists come to you with ideas, or do you ask them to visualize something you want to write about?
I wish I had artists. When I started “Krulwich Wonders,” I did. I had a little budget and could hire people to help me. But those were the early days when managers were given play money to launch these adventures. The play period has long since ended and now I’m down to me, my box of colored pencils, my desk top scanner and an eraser. I can still call friends, and I do, and I will, but mostly I sit there thinking about, oh, I don’t know, “snail sex,” and I end up looking up pictures of snails, trying to find their genitalia (not the easiest thing to do if you’re not a snail) and sitting at my desk drawing one lopsided snail after another until, eventually, I get the thing right plausibly snaily enough and anatomically correct enough to publish. Then if my wife happens by, sees the drawing, and says, “Oh, what a nice pineapple,” I start over.
The ideas, by the way, come from whatever it is I’m wondering about.
What’s your favorite blog post so far? (Disclosure: my favorite is the one you wrote about the giant insects that were rediscovered on a remote island.)
Thanks, I liked that one too. But if I had to choose, I’d nominate one I wrote about why bees love hexagons, which you can find here. Or another about bees being totally and mysteriously absent from a cornfield, or this short meditation on absolutely nothing. And, oh yes, a dance I posted that still makes me so happy I use it like alchohol whenever I’m gloomy. It’s here.
What’s your plan for blogging from here on out?
To try things I’ve never tried before. To scare myself. To experiment with newfangled gifs, loops, slo-mo photography, and, if I dare, watercolor. To go wherever my curiosity takes me, and to take you (that’s right, I’m whispering in your ear, Carl Zimmer, you who know everything I know several weeks before I do), even you are coming with me.
My bags are packed.
May 28, 2015
Save the Zombie-Makers!
Parasites may seem too gross or too wicked to be worth saving from extinction. Or they may just seem so skilled in their sinister arts that we don’t have to worry about them, since they’ll always find a new victim.
In fact, parasites warrant our concern, right along with their hosts. That’s not to say that we’d better off if smallpox or rinderpest were still running wild. But letting parasites hurtle into oblivion due to our ecological recklessness is a bad idea.
Here’s a case in point: The World Wildlife Fund has just drawn attention to a parasitic wasp, Ampulex dementor, that makes cockroaches its zombified victims. The wasp was found in 2007 in Thailand, and in 2014 a German museum held a contest to give it a species name. Museum goers voted to name it after the soul-sucking dementors in the Harry Potter series.
WWF highlighted A. dementor in a new report on the 139 new species from the Greater Mekong Region that were described in 2014 alone. This region, which includes Cambodia, Laos, Myanmar, Thailand, and Vietnam, is stunningly rich with species. It’s also incredibly productive, yielding a quarter of the world’s catch of freshwater fish. But it’s also under intense pressure, ranking in the top five threatened biodiversity hotspots on Earth. Dams, roads, logging, and hunting are all taking their toll on the species there. Climate change will only add to the threats the Mekong’s species face.
A species like A. dementor is caught in a special bind. We didn’t even know it existed until recently, so it’s hard to know precisely how well the species is faring. No one has a detailed map of its range before human pressure ramped up in the past century, and no one has a corresponding map of its current range.
On top of that, the published scientific literature–pretty much just a single paper published last year–doesn’t even tell us about the particular cockroaches the wasp parasitizes. Does it zombify several species of cockroaches? Does it zombify just one? These questions matter a lot to the survival of A. dementor. If it parasitizes a single rare species, it could become extinct if its host disappears. (While a few species of cockroaches have become global champions by adapting to our homes, the vast majority can only survive in wild forests.)
While we know little about this parasite, the ecological threats to the Greater Mekong Region should make us concerned about it. And losing a species of parasite can be a bad thing. Parasites, for example, are important players in food webs. If they disappear from an ecosystem, their hosts–and the species that are affected by those hosts–may undergo wild swings. If you don’t like cockroaches, the last thing you want is for the parasites that devour them from the inside out to vanish.
Parasites are also worth saving for what they have to teach us. And that’s especially true for wasps like A. dementor. It belongs to a lineage known as Ampulicidae or the cockroach wasps, which contains 200 named species–and probably many more waiting to be discovered. The best known of these species is Ampulex compressa, sometimes called the emerald cockroach wasp. Phenomena readers may be quite familiar with the emerald cockroach wasp, because fellow blogger Ed Yong and I just won’t shut up about it. (I also added an epilogue to my book Parasite Rex pretty much just to write about it.)
The reason we know so much about the emerald cockroach wasp is that a team of researchers led by Frederic Libersat at Ben-Gurion University in Israel have figured out how to rear the wasps in their lab, and for years now they’ve been observing its remarkable skills.
The female emerald cockroach wasp searches for roaches, probably scanning the ground while sniffing the air. The wasp swoops down on the roach and stings it in its abdomen, temporarily paralyzing it. It then delivers a second shot to the head–literally snaking its stinger into the recesses of the cockroach brain. Now the cockroach loses all motivation to do much of anything. You can even shock its leg and it won’t budge on its own. But the wasp can grab onto an antenna and lead it into a burrow.
There, the wasp lays an egg on the roach’s underside and then leaves, sealing the burrow behind it. The egg hatches and the larva sucks on the roach in tick-like fashion for a while, before squirming inside the host’s body to finish off its growth. To keep its host from dying of infections, it smears an antibiotic cocktail on the roach’s inner body wall. The wasp larva forms a cocoon inside the roach, which then finally dies. Later, the fully-grown wasp pokes its head out of the roach, wriggles entirely free, and leaves the burrow.
These wasps may have many lessons for us. Most of their antibiotics are new to science, for example, and so they may be worth investigating further for medicine. The wasps have also evolved a remarkable skill at manipulating the cockroach brain. Figuring out how they do it might tell us more about how the nervous systems of insects work. And it might provide some inspirations for ways to manipulate our own brains–not to turn ourselves into zombies, but to treat psychological disorders.
But almost all the insights we’ve got about cockroach wasps come from a single species. Far from being degenerates, as they were traditionally viewed, parasites can evolve rapidly, hitting on new strategies for conquering their hosts. So it’s entirely possible that A. dementor uses a soul-sucking arsenal that’s significantly different than its cousin species A. compressa. The only way we can enjoy discovering that arsenal is to make sure this species doesn’t vanish first.
****
If you want to find out more about cockroach wasps, here are some pointers:
Me at TED-Ed, grossing out high schoolers with the details of the emerald cockroach wasp:
Ed at TED, talking about wasps and other parasitic mind-controllers:
Here’s a post I wrote in 2006 after a scientist first told me about Ampulex compressa, and after I confirmed he wasn’t just trying to fool me into thinking a crazy story was true.
Here’s Ed on how the wasp’s venom affects cockroach behavior.
Me on parasite antibiotics, and Ed’s write-up in Nature.
Me on how the wasps snake their stinger through the cockroach brain.
And on Radiolab, I talk to Jad Abumrad and Robert Krulwich about how these wasps put science fiction to shame.
May 27, 2015
The Mystery of Kangaroo Adoptions
When you spend five years watching kangaroos, you start to see some strange things. From 2008 to 2013, Wendy King, a biologist at Bishop’s University in Quebec, and her colleagues studied wild grey kangaroos in a national park in Victoria, Australia. All told, King and her colleagues studied 615 animals–194 adult females, and 326 juveniles, known as joeys. The first time King and her colleagues captured each kangaroo, they took a number of measurements and then marked it so they could recognize it later. From time to time, they’d find a juvenile kangaroo in the pouch of a different mother. Sometimes it would climb out, but then it would climb back into the new pouch, getting milk and protection from the adult female for months, until it was ready to live on its own.
In other words, these kangaroos had been adopted.
A marked kangaroo and her adopted joey. King et al PLOS One 2015 http://bit.ly/1dxRljP
Scientists have observed adoption in occurring 120 species of mammals. Other species that are harder to study may be adopting, too. As for kangaroos, scientists have long known that if they put a joey in an unrelated female’s pouch, she will sometimes keep it. But King and her colleagues have now discovered that kangaroos will voluntarily adopt joeys in the wild. All told, they found that 11 of the 326 juveniles were adopted over their five-year study–a rate of about three percent. Given the commitment adoption demands from a mammal mother–a kangaroo mother needs a full year to raise a single joey to weaning–this discovery cries out for an explanation.
Over the years, researchers have proposed a number of different explanations for adoption. Some have suggested that mammals adopt young offspring of their relatives because they are genetically similar. By rearing the offspring of their kin, this argument goes, adoptive parents can ensure that some of their own genes get passed down to future generations.
According to another explanation, unrelated adults may adopt each other’s young because this kind of quid-pro-quo benefits everyone involved. And according to a third explanation, young adults adopt orphaned juveniles as a kind of apprenticeship. They learn some important lessons about how to raise young animals, which they can apply later to raising their own offspring.
These explanations share something in common. They all take adoption to have an evolutionary benefit. In the long run, the genes that make animals willing to adopt become more common thanks to natural selection.
But in the case of kangaroos–and perhaps other species, too–evolution may have instead have made a mess of things. Adoption may not be an adaptation. It may be a maladaptation.
To understand why some kangaroos adopted joeys, King and her colleagues looked for evidence that adoption provides an evolutionary benefit. They found that adoptive mothers didn’t pick out closely related juveniles to adopt. That finding weighs against kinship as an explanation.
King and her colleagues also didn’t find evidence to support the adoption-as-practice explanation. For one thing, only one out of eleven adoptive mothers was a young female that hadn’t yet had joeys of her own. In fact, some of the mothers swapped their babies.
Remarkably, King and her colleagues never observed an orphaned juvenile being adopted. In some cases, a mother adopting one joey would, in the process, abandon her own. These abandoned joeys were not then taken up by another adult female. Instead, they disappeared, presumably killed by foxes or other predators in the park.
All in all, adoption seems like a pretty bad move for mothers and joeys alike. King and her colleagues propose that adoptions happen not because natural selection favors it, but because kangaroos aren’t very good at recognizing their own joeys.
When a joey climbs out of its mother’s pouch and then tries to hop back in, its mother gives it a sniff. If the joey doesn’t smell like it belongs to her, she will push it away. King and her colleagues propose that in an emergency–such as when a predator turns up, prompting joeys to rush into pouches and adults to hop away–mothers may not have time for this inspection. An unrelated joey may leap in their pouch and stay there as the mother flees for safety. Once in the pouch, the joey will take on the same odor as her own offspring had. Now it will pass the sniff test–and become officially adopted.
One observation that King and her colleagues made supports this explanation: adoptions happened more often when the kangaroo population was high. When a mother is surrounded by a big crowd of joeys, there may be more opportunities for an unrelated joey to leap into her pouch.
I asked Kirsty MacLeod, a biologist at the University of Cambridge, what she thought about the new study. She found the evidence compelling, if bizarre. “It’s pretty weird,” she said. “It makes very little evolutionary sense to stop investing in your own young, and instead divert all your resources to another offspring, especially one that isn’t related to you.”
MacLeod thinks King is probably right that kangaroos adopt by accident during a crisis. “But that doesn’t necessarily mean it’s intrinsically nonadaptive,” she added.
Grabbing the closest joey in an emergency may be a good strategy for kangaroo mothers, since the closest joey will probably be her own. “It’s likely better to take that chance (and one out of ten times, face the consequence of raising another female’s young),” said MacLeod, “than to risk separation and offspring death, a catastrophe for a mother that spends over a year rearing a joey.”
It would be a mistake to draw a lot of lessons from this study about human nature. It’s true that humans adopt children, too. But the causes behind human adoption demand attention to the human experience–which, among other things, does not involve putting babies in pouches. But there are other lessons to take from this research. When trying to make sense of the weirdness of animal behavior, it’s a good idea to consider the possibility that it exists because of its evolutionary benefit. But it’s also worth wondering if you’re dealing with evolution’s imperfection.
