Dr. Christie Wilcox is a science writer based in the greater Seattle area. Her bylines include National Geographic, Popular Science, and Quanta. Her debut book, Venomous, released August 2016 (Scientific American/FSG Books). To learn more about her life and work, check out her webpage or follow her on Twitter, Google+, or Facebook.
Lots of animals use chemical cues to avoid danger. Mice will run from the smell of cat urine, for example. But one particular instance of chemical fear signaling has been stumping scientists for 70 years; the release of Schreckstoff by schooling fish.
For some species of fish, when a predator swoops in and injures one fish in a school, the rest will take off in fear. This much we know. In 1938, Austrian ethologist Karl von Frisch claimed that at the root of this behavior was a chemical alarm signal which he referred to as “Schreckstoff,” which means “scary stuff” in German. Since von Frisch’s seminal work, over 100 published studies concerning Schreckstoff have demonstrated that certain fishes have some substance in their skin cells which is released when that fish is injured and causes other fish to scatter. That much, we know, too.
This has perplexed scientists because it seems strange that any animal could evolve to give off that kind of chemical alarm. The other fish aren’t fleeing from blood or any clear signals of death, so what are they so afraid of? And if it’s not a signal of death but instead a signal of danger, as many scientists have argued, where is the benefit to the dying fish? You see, as much as we love the idea of altruism, it’s not very common in the natural world – at least not in its pure form. Doing something purely for the sake of others is of little benefit to an individual from an evolutionary perspective. So, hypotheses have been thrown around wildly to explain this kind of altruistic signaling – perhaps the alarm is to protect close kin, or, somehow, the chemical actually attracts the would-be-predator’s predators, thus giving the injured fish a chance to escape. Despite years of laboratory research, no hypothesis seems to be able to explain the presence of Schreckstoff. Furthermore, though some scientists have offered up potential compounds, what exactly Schreckstoff is has remained a mystery.
Chondroitin sulfate is a specialized chain of sugars that is a major component of fish skin, just like it’s a major component of our cartilage. Using zebrafish, a common laboratory organism, the research team found chondroitin from zebrafish tissues caused other fish to turn fin and run. They even took chondroitin from shark skin – the kind we take as supplements – and found that the zebrafish were terrified by it. The fish were also more afraid when the chondroitin was broken down by an enzyme first. The team hypothesized that when a fish is injured, enzymes released by the wounding break down chondroitin sulfate into smaller sugary chunks, and these bits and pieces, as well as the larger chondroitin molecules released by the wounded cells, are the smell that serves as a chemical alarm signal.
The best part of this discovery is that it solves evolutionary issue that scientists have had with the existence of Schreckstoff. The burden of producing a fear signal while dying doesn’t make sense unless that signal is something the fish already produced for other reasons which is only released in the case of injury – akin to some being afraid of the smell of blood. That way, the evolutionary impetus isn’t on the fish producing Schreckstoff to produce an alarm, it’s on other individuals to detect a sign of danger or death to save their own tails.
Here’s how it goes: once upon an evolutionary time, fish that were sensitive to Schreckstoff were the first to run in the face of danger, and thus were more likely to survive. Over time this would lead to an entire lineage of Schreckstoff-sensitive fish. Since chondroitin is a known component of fish skin for other reasons, but wouldn’t be released into the water unless that skin is ruptured, it perfectly fits this evolutionary scenario.
Because young zebrafish are see-through, researchers were also able to specifically examine what parts of the zebrafish brain are turned on by chondroitin fragments. They found that a specialized part of the brain called the mediodorsal posterior region was responsible for the fearful reaction. What is particularly interesting about this chunk of brain matter is that it is packed with a group of neurons called crypt cells which have no other known function. Scientists have been trying to uncover what these strange neurons do for awhile, and this new discovery may hold the key. Co-author Suresh Jesuthasan thinks that these cells are a part of a special brain circuit which mediates the fish’s innate fear response.
Together, the new findings, published in Current Biology, are the pieces to the Schreckstoff puzzle that scientists have been trying to fit for decades. There are still questions to be answered, of course – how do certain species only respond to injuries by their own species and not those of others, for example? – but this new study has provided valuable insight into fear responses in fish, and perhaps opened up new doors in our understanding of how fear originates and is processed in animal brains.
Article Link: Mathuru et al., Chondroitin Fragments Are Odorants that Trigger Fear Behavior in Fish, Current Biology (2012), doi:10.1016/j.cub.2012.01.06
Here’s the researchers’ video of the fear response:
153 years ago on November 24th a naturalist named Charles Darwin published a book with a rather long and cumbersome title. It was called On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life (for its sixth edition in 1872, the title was cut short to simply The Origin of Species, which was found to be much more manageable to say in conversation). It was inspired by an almost five year journey around the world on a ship named for a small, floppy eared canine during which Darwin did his best to catalog and understand geology and the diversity of life he found.
It’s incomprehensible, now, to think of someone writing a single volume that could equally change science as we know it. The two simple ideas that Darwin fleshed out in his first publication were earth shattering at the time. He has since been called both a genius and a heretic for these two theories – both titles equally deserved. But whatever you call him, his vision has changed the world irrevocably. Today, on what would have been his 203 birthday, we celebrate the life and scientific contributions of this man. In honor of the occasion, I am reposting my first Darwin Day post ever, from way back in 2009. Enjoy!
If I ask you what group of organisms is an exhibition of evolution at its finest, what would you say? Most people, I think, would say human beings, or at least apex predators. After all, we have staggering intellect compared to our prey items and clearly dominate the planet, eat what we will, etc. Not only that, we’re insanely complex. Ask some scientists, and they might give you any number of answers. Cockroaches are likely to exist long after we do, as are rodents, so maybe they get the title. Or, being scientists, they might be biased to whatever organism they study. Maybe algae and plants, as the sustenance for all other life. But all of you, in my humble opinion, are wrong. That is, unless you choose parasites.
It’s ok if you don’t believe me yet. Darwin wouldn’t have, either. He and his contemporaries viewed parasites as degenerates who, at best, violated the progressive nature of evolution. Even in The Origin of Species, Darwin refers to parasites as regressive instead of progressive. But truly, no group of species is a better choice for evolution’s finest.
First off, let’s talk numbers. Parasitism is the most popular lifestyle on earth – over 40% of all known species are parasitic, and the number of parasitic species rises daily1. Sure, you might say, but they tend to be small. In that case, let’s talk biomass – weight, just to be clear. One group of parasites, the flukes, have been found to be equal in weight to fish in estuarine habitats, and three to nine times the weight of the top predators, the birds – estimates which are thought to be conservative for the earth as a whole2. Though they’re largely ignored when we study food webs, they’ve been estimated to be involved in over 75% of inter-species interactions1. Clearly, by the numbers, they are the most prolific and successful organisms on earth.
But even that is not why I would argue they are evolution’s finest. They, more than any other group out there, both exhibit extreme evolutionary adaptations and spur them onward in other species.
No matter how complex or how impressive any other species may be, it has parasites. We do – lots, actually. Every species we might hold as a masterpiece of evolutionary complexity cannot out maneuver their parasites. Not one. Even parasites, marvelous as some are, have parasites – like a crazy russian doll. They have evolved amazing abilities to survive host defense systems, manipulate host behavior and boost heir own reproductive success. They’ve even been implicated in major cultural differences in people. It turns out that a rat parasite, Toxoplasma gondii, needs to be eaten by a cat to complete its lifestyle. Somehow it developed a trick to make rats unafraid of cat smells. When it accidentally ends up in people, it does the same kind of mind-altering, making people more guilty and insecure, even more frugal, mild-tempered, and complacent3. Other parasites do far more intricate manipulations of behavior, turning males into females, creating walking zombies, even forcing suicide. If parasites can not only break into and survive the most complex assortments of systems available, even with modern medicine fighting against them, and manipulate those complex organisms to slave to their bidding, how can we not credit them as masters at what they do?
But even more impressively, I would argue, is that no other group has so dramatically impacted how other species have evolved. They don’t just affect their hosts immune systems, either. If you read much into evolutionary theory, you realize it’s riddled with parasites. Why are some birds very colorful? Oh, because if they’ve got a lot of parasites they can’t be, so it’s a signal of a healthy male4. Why are we attracted to certain people? Because their immune genes are different from ours, giving our children the best chance to fight off the next generation of parasites. Almost everywhere you look, evolutionary changes are spurred on by parasites. It’s even suggested that sex itself evolved as a response to parasites. It’s a way of better shuffling our genes so that we have better odds at fighting off parasites.
Even we, as “ideal” or “complex” as we are, owe much to parasites. Some even argue that we are worse off without them. The argument, as it goes, is that our immune system evolved in the presence of unkillable parasites, particularly the parasitic worms. These worms, or Helminths as they are called as a group, were too costly to try and eradicate. Attacking foreign invaders, after all, is energetically expensive, and always runs the risk of over-activating our immune system, leading to self-inflicted injuries and diseases. So the best strategy, instead, was to have an immune system that functioned optimally against other issues, like the fatal viruses or bacteria, despite the mostly benign worm infections5. Since worms secrete anti-inflammatory compounds to fight off our defenses, we were better off with systems that overcompensated for that. Now, since we have drugs which kill them off, our immune system is out of balance. Many cite the rising rates of auto-immune and inflammatory diseases like allergies, arthritis, irritable bowel, type 1 diabetes, and even cancer in developed nations as evidence that ridding ourselves of helminths has damaged our health6. They’re backed up with multiple studies that show unexpected results, like that mice genetically predisposed to diabetes never develop it if infected with flukes at an early enough age.7
Parasites are uniquely capable of out-evolving their hosts and adapting to whatever changes go on in them. Simply put, they evolve better. They change their genes faster and keep up with a barrage of host defense systems, often like it’s effortless, spurring onward dramatic changes in other species. If Darwin had only known how amazingly complex the barriers these creatures have to overcome and the extent to which they have affected the species he’d encountered on his travels, he would not have labeled them “degenerates”.
As far as evolution is concerned, no group of species demonstrates it, causes it, and is so capable of it as the parasites. While disgusting or even cruel, they are truly evolutionary masterpieces. So while you may find them vile or detestable, you have to admit they’re good at it. Can you really argue that some other group is more deserving of the title of Evolution’s Finest?
Cited: 1. A. Dobson, K. D. Lafferty, A. M. Kuris, R. F. Hechinger, W. Jetz (2008). Colloquium Paper: Homage to Linnaeus: How many parasites? How many hosts? Proceedings of the National Academy of Sciences, 105 (Supplement_1), 11482-11489 DOI: 10.1073/pnas.0803232105
2. Armand M. Kuris, Ryan F. Hechinger, Jenny C. Shaw, Kathleen L. Whitney, Leopoldina Aguirre-Macedo, Charlie A. Boch, Andrew P. Dobson, Eleca J. Dunham, Brian L. Fredensborg, Todd C. Huspeni, Julio Lorda, Luzviminda Mababa, Frank T. Mancini, Adrienne B. Mora, Maria Pickering, Nadia L. Talhouk, Mark E. Torchin, Kevin D. Lafferty (2008). Ecosystem energetic implications of parasite and free-living biomass in three estuaries Nature, 454 (7203), 515-518 DOI: 10.1038/nature06970
3. Kevin D. Lafferty (2006). Can the common brain parasite, Toxoplasma gondii, influence human culture? Proceedings of the Royal Society B: Biological Sciences, 273 (1602), 2749-2755 DOI: 10.1098/rspb.2006.3641
4. Jesús Martínez-Padilla, François Mougeot, Lorenzo Pérez-Rodríguez, Gary R. Bortolotti (2007). Nematode parasites reduce carotenoid-based signalling in male red grouse Biology Letters, 3 (2), 161-164 DOI: 10.1098/rsbl.2006.0593
5. Joseph A. Jackson, Ida M. Friberg, Susan Little, Janette E. Bradley (2009). Review series on helminths, immune modulation and the hygiene hypothesis: Immunity against helminths and immunological phenomena in modern human populations: coevolutionary legacies? Immunology, 126 (1), 18-27 DOI: 10.1111/j.1365-2567.2008.03010.x
6. Joel V. Weinstock, David E. Elliott (2009). Helminths and the IBD hygiene hypothesis Inflammatory Bowel Diseases, 15 (1), 128-133 DOI: 10.1002/ibd.20633
7. Anne Cooke (2009). Review series on helminths, immune modulation and the hygiene hypothesis: How might infection modulate the onset of type 1 diabetes? Immunology, 126 (1), 12-17 DOI: 10.1111/j.1365-2567.2008.03009.x
All of this is why I completely and totally love the new tumblr This Is What A Scientist Looks Like started by sci-comm guru Allie Wilkinson. Scientists from all kinds of fields are asked to submit photos of themselves and write a brief bit about who they are. The pictures are incredible; scientists are depicted everywhere from Antarctica to the tropics, on the tops of mountains or under the sea. The pics express personality, intelligence, and even a little humor.
Anyhow, if you’re a scientist, I strongly encourage you to add yourself. And if you’re not, go check out what scientists really look like, including a few goofballs like this:
In the wake of Science Online 2012, a new hashtag has emerged on twitter: #Iamscience.
I, too, am science. A few years ago, when I was about to begin my PhD, I wrote my I Am Science story. I am reposting it now, in honor of the hashtag. If you’re on twitter, definitely check out all the great stories being told!
A Marine Biologist’s Story
The air felt thick and heavy in my lungs. As I drove further down the narrow strip of beach, my throat closed and my eyes burned. It wasn’t normal sea air – it was toxic. Red tide was hitting the area in full force, killing off thousands of marine animals and filling the air with the neurotoxic compounds the algae Karenia brevis is known for. As the waves crash on shore, they break open the delicate algal cells, aerosolizing the odorless but noxious brevatoxins.
Many people have heard of red tide, but if you haven’t experienced it, you should consider yourself lucky. A few years ago I was driving an ATV on Casey Key late at night looking for nesting turtles to tag during one of the worst red tide seasons in recent history. Everything was dying. You couldn’t go near a beach without coughing and wheezing, and you probably didn’t want to anyhow, since they were covered in dead fish and other marine life.
But there I was, 2:30 in the morning, holding my breath as much as I could and scanning relentlessly for nesting turtles as a part of a summer internship at Mote Marine Laboratory in Sarasota, FL. I hadn’t slept much in days, and I was going to be out there until sunrise. I was exhausted. I couldn’t breathe. And it was in that moment that I started thinking about how I ended up in this situation in the first place.
You know, no one ever asks me why I am a marine biologist. I still expect that people will, and that I’ll get to tell these elaborate stories of the great things I get to do as if they had anything to do with my choice to follow this career path. But no one ever asks. I think most people assume that they know why someone becomes a marine biologist. They think “ooo, she gets to be like those people at SeaWorld riding the dolphins.” Everyone has this fanatasy of what a marine biologist is, and they think that all marine biologists have known their whole lives they would end up that way.
First off, they’re completely wrong about what it means to be a marine biologist. Being a marine biologist isn’t all playful dolphins and spectacular diving. It’s driving an ATV up and down a beach littered with dead fish – and spending an hour pulling a 200 lb dead sea turtle high enough out of the water so that the stranding crew could find it in the morning, even though you can barely breathe. It’s never, ever being able to look at seafood the same way again. It’s getting up at a god-awful hour to make it to your field site for sampling when the tide is at just the right height, where you can pull water from the ground but still count the crab burrows on the surface, then staying out there all day even though it’s 100 degrees out with no clouds and you feel like you’re being baked alive. It’s cleaning the bones of a manatee so that it can be used as a teaching tool, which requires placing the putrid rotting skeleton in a vat of water in the sun to rot, and then going back once a week, dumping the fetid water and pulling whatever decomposed flesh you can off, until the bones are picked clean. It’s counting the 53 dead baby sea turles from a nest that was raided by fire ants (who aren’t exactly pleased that you’re disturbing their hard-earned meal). It’s staring into a microscope for hours picking the miniature, formaldehyde-pickled marine life from a mud sample to catalog the fauna in a riverbed. It’s always feeling like you smell of dead creatures or harmful chemicals, and being so used to it you actually kind of like the smell.
In other words, it’s gruesome. It’s a little grotesque. And to be honest, there’s got to be something kind of off with you to begin with to enjoy it enough to make a living doing it.
Secondly, I haven’t always known I would be a marine biologist. Looking back it might be obvious to the casual observer, but that doesn’t mean it was obvious to me. I didn’t really figure it out until I had to pick a college and a major to go with it. Let me explain:
I was born in Boston, Massachusetts in the summer of 1985. I was happy in New England. I liked being a little kid. And I was a smart kid, too, which made being a little kid all the more fun. I didn’t really have much of a choice about being nerdy. Just look at my dad, who designed the first computer go program – I was screwed. Neither of my parents, though, were biologists, and in Boston the ocean is cold and unwelcoming. Of course, when I was about four years old, my parents decided they didn’t want to live in the frozen northeast any more, and they moved me and my brother to Hawai’i. I know – how awful.
It’s in Hawai’i that the first signs of my future career began to show. At the ripe age of 5 years old, my parents decided to send me to a special school for gifted kids (I said I was smart, didn’t I?).
I liked tongues.
To do so, they had to have my IQ tested. I passed. But the most interesting part of my IQ report isn’t the score, it’s the commentary from my examiner. She said I was a “poised, cooperative young child.” I was friendly and quick to talk, and even better, in my chatty childish way, I talked about what I liked:
The student spoke briefly about her interest in animals and bugs, noting that she likes to “find dead geckos and open their mouths to see their tongues.“
Oh yeah. I was a biologist when I was five – not that I knew this until much later. I loved animals of all kinds, and couldn’t get enough of museums and zoos. I also fell in love with the sea. I loved tide pools and whatever creatures I could find in them. I thrived in the ocean, learning to swim at a very young age and spending as much time as I could underwater instead of on land. Hawai’i became my home, and I felt like I had lived there all my life (I still say “Hawai’i” and certain Hawaiian and Asian words with an accent that never ceases amuses my non-local friends).
Then my parents divorced. My mom moved to Vermont, of all possible places. So I spent most of the year in the artic world of New England, and only my summers back in the wet and salty world I loved. But being in Vermont gave me the opportunity to explore a whole range of interests. Being an outgoing person, I took well to the stage, and loved every facet of the theater. I loved art and painting, and always had a creative streak in me that I still nurture. I learned to play guitar and sing, and wrote my own songs. By high school, in fact, you probably would have expected me to end up a starving artist of some kind.
In high school, I was a jack of all trades. I took the highest level courses in math, science, theater, art, history, and english. My senior year I was granted independent studies in History, Theater and English. I took all kinds of AP courses, walking away with APs in English Lit, English Language, U.S. History, Calculus BC, Physics B and Advanced Physics. Note, for the record, that not one of the things I just mentioned has the word “biology” in it.
You see, I loved animals – I had cats and dogs and odd pets like hedgehogs my whole life, I loved searching the woods for living creatures, adopting anything injured or sick – but I didn’t think of myself as a biologist. Not yet, anyhow. I was an actress, musician, artist, writer, historian, and even physicist, but I wasn’t a biologist. Then, of course, I had to think about where I wanted to go to college. There was one thing I wanted above all else – I wanted to live in Hawai’i.
I missed it. I missed the water and the waves. I missed the sun and the beach. I missed everything about the islands. I felt like a fish out of water in New England – all I wanted was to go home.
Somehow, in my homesick, 16-year-old mind, I came up with a brilliant idea. I would study the physics of cetacean (whale and dolphin) communication. I could double major in Marine Biology and Physics, ending up in Hawai’i for graduate school, and I would get to be where I belonged. So I found out which colleges had good science programs, particularly marine ones (the whole getting back to Hawai’i bit hinged on me being a marine-centered physicist), and applied. And through a twist of fate, I ended up in Florida at Eckerd College.
After my first semester of courses at Eckerd, though, I knew that I wasn’t a physicist. I loved physics, but the advanced, theoretical stuff just wasn’t my cup of tea – I liked the hands on, applied physics. I did, however, adore my marine science classes. I liked learning about the physiology of marine inverts, and playing with them in labs. Once, I spent an entire hour flipping an upside-down jellyfish upside-down then right-side-up again until my hand actually went numb. I met my undergraduate mentor, Dr. Nancy Smith, who I quickly came to aspire to be like. And from that time onward, there was no doubt in my mind that although I didn’t know it until then, I was a biologist all along.
I believe the phrase is, “duh”
In truth, I should have seen it earlier. Heck, I was never squeamish or easily grossed out by things. When I took freshman biology in high school I was the only person who actually got a bit of a kick out of dissecting the fetal pig. I stayed after class to carefully remove its brain so that I could look at it close-up. I loved the natural world. I really, really loved animals, often to my parents’ dismay when I would attempt to make “pets” out of every creature I could get my hands on. When I was writing my PhD applications this year, I asked my dad when he knew that I would end up in biology. “Are you kidding me?” he responded. “You’ve been like this since you were born!”
But I didn’t become a marine biologist because I wanted to since birth. I didn’t even want to since I was in high school. In some ways, I became a marine biologist by accident. Or maybe it was fate, if such a thing exists.
Now, I can’t imagine a life other than this. I love what I do. You see, it was that thought, not some self-doubting “why am I doing this?”, which went though my head as I breathed in the thick, noxious air while riding that ATV. It was a thought of wonder, asking the world how I got to be so lucky as to do what I do. In truth, I was barely paying attention to the toxic fumes. I was too intrigued by the fact that the dead fish I drove over started to glow after my tires crunched their bones – the beach, in fact, was glowing bluish-green. Some kind of bioluminescent algae or bacteria was all over the rotting corpses and in the water, and it glowed whenever it was disturbed. It was one of the coolest things I’d ever seen. I remember stopping just to step on dead fish and watch them light up (I did say you have to be a little sick to do what I do, right?).
Of course, the best part was tagging the turtles. That night I sat quietly and watched massive female green sea turtles dig their nests and drop hundreds of eggs into the sand. While they did, of course, I calmly checked their flippers for tags and tagged any that didn’t have them already. They didn’t run or flee as I touched them – once a female sea turtle has begun laying her eggs, she’s intent on finishing the job, and just about nothing will deter her from that task. To this day, the sight of those beautiful girls laying their precious eggs is still one of my favorite memories.
The point, I guess, of this long and self-indulgent monologue is that you should always follow your passions, and eventually, you’ll end up where you want to be. Or where you want to be will be where you end up – as Douglas Adams says, “I may not have ended up where I intended to go, but I know I’ve ended up where I’m intended to be.” For me, in the end, I even get to fulfill my 16-year-old me’s dream – in the fall, I start my PhD at the University of Hawaii.
This story is also in part to explain what it means to be a marine biologist. It’s not all cliches and playful creatures, and we’re all a little weird to even like what we do. And in part, I wanted you all to get to know me a bit better.
But mostly, it’s because no one ever asks why I’m a marine biologist. I have all these fun stories and anecdotes about being nerdy. And, damn it, I really wanted to tell some of them.
Whew. What a crazy week! Just 7 days ago, I hopped on a plane and began my long journey eastward to North Carolina to attend Science Online 2012. In case you aren’t familiar with the conference, Science Online is, as Christopher Mims said, like “a Burning Man for Science Journalists.” For me, this meant three days straight of talking, learning, and networking – note the absence of the word “sleeping.” Last night was the first time in a week I got more than 5 hours sleep. It was amazing.
Anyhow, I was at Science Online not only to engage with other scientists and journalists, but also to co-moderate a session titled “Blogging Science While Female.” Here’s the session description:
The session on women in science blogging at Science Online 2011 sparked internet-wide discussion about sexism, discrimination and gender representation in science and science blogging. Now here we are, a year later. How have we, as a community, faced the issues brought up by last year’s discussion? What has changed? What have we learned, and what challenges still lie ahead? Moderators and attendees will assess the current state of women in the science blogosphere and discuss the best way we can support and encourage gender representation in science blogging.
Rather than rehash the session here, I’ll instead give you Tanya Lewis’ storify of the session (below). Also, be sure to read Kate Clancy’s epically awesome post: Blogging While Female, and Why We Need A Posse
Let’s rewind time back about 3.5 billion years. Our beloved planet looks nothing like the lush home we know today – it is a turbulent place, still undergoing the process of formation. Land is a fluid concept, consisting of molten lava flows being created and destroyed by massive volcanoes. The air is thick with toxic gasses like methane and ammonia which spew from the eruptions. Over time, water vapor collects, creating our first weather events, though on this early Earth there is no such thing as a light drizzle. Boiling hot acid rain pours down on the barren land for millions of years, slowly forming bubbling oceans and seas. Yet in this unwelcoming, violent landscape, life begins.
The creatures which dared to arise are called cyanobacteria, or blue-green algae. They were the pioneers of photosynthesis, transforming the toxic atmosphere by producing oxygen and eventually paving the way for the plants and animals of today. But what is even more incredible is that they were the first to do something extraordinary – they were the first cells to join forces and create multicellular life.
It’s a big step for evolution, going from a single cell focused solely on its own survival to a multicellular organism where cells coordinate and work together. Creationists often cite this jump as evidence of God’s influence, because it seems impossible that creatures could make such a brazen leap unaided. But scientists have shown that multicellularity can arise in the lab, given strong enough selective pressure.
Just ask William Ratcliff and his colleagues at the University of Minnesota. In a PNAS paper published online this week, they show how multicellular yeast can arise in less than two months in the lab. To achieve this leap, they took brewer’s yeast – a common, single celled lab organism – and grew them in a liquid medium. Once a day, they gently spun the yeast in the culture, starting the next batch with whichever cells ended up at the bottom of the tube. Because the force of spinning pulls larger things down first, clumps of cells were more likely to be at the bottom than single ones, thus setting up a strong selective pressure for multicellularity.
All of their cultures went from single cells to snowflake-like clumps in less than 60 days. “Although known transitions to complex multicellularity, with clearly differentiated cell types, occurred over millions of years, we have shown that the ?rst crucial steps in the transition from unicellularity to multicellularity can evolve remarkably quickly under appropriate selective conditions,” write the authors. These clumps weren’t just independent cells sticking together for the sake of it – they acted as rudimentary multicellular creatures. They were formed not by random cells attaching but by genetically identical cells not fully separating after division. Furthermore, there was division of labor between cells. As the groups reached a certain size, some cells underwent programmed cell death, providing places for daughter clumps to break from. Since individual cells acting as autonomous organisms would value their own survival, this intentional culling suggests that the cells acted instead in the interest of the group as a whole organism.
Given how easily multicellular creatures can arise in test tubes, it might then come as no surprise that multicellularity has arisen at least a dozen times in the history of life, independently in bacteria, plants and of course, animals, beginning the evolutionary tree that we sit atop today. Our evolutionary history is littered with leaps of complexity. While such intricacies might seem impossible, study after study has shown that even the most complex structures can arise through the meandering path of evolution. In Evolution’s Witness, Ivan Schwab explains how one of the most complex organs in our body, our eyes, evolved. Often touted by Intelligent Designers as ‘irreducibly complex’, eyes are highly intricate machines that require a number of parts working together to function. But not even the labyrinthine structures in the eye present an insurmountable barrier to evolution.
Our ability to see began to evolve long before animals radiated. Visual pigments, like retinal, are found in all animal lineages, and were first harnessed by prokaryotes to respond to changes in light more than 2.5 billion years ago. But the first complex eyes can be found about 540 million years ago, during a time of rapid diversification colloquially referred to as the Cambrian Explosion. It all began when comb jellies, sponges and jellyfish, along with clonal bacteria, were the first to group photoreceptive cells and create light-sensitive ‘eyespots’. These primitive visual centers could detect light intensity, but lacked the ability to define objects. That’s not to say, though, that eyespots aren’t important – eyespots are such an asset that they arose independently in at least 40 different lineages. But it was the other invertebrate lineages that would take the simple eyespot and turn it into something incredible.
According to Schwab, the transition from eyespot to eye is quite small. “Once an eyespot is established, the ability to recognize spatial characteristics – our eye definition – takes one of two mechanisms: invagination (a pit) or evagination (a bulge).” Those pits or bulges can then be focused with any clear material forming a lens (different lineages use a wide variety of molecules for their lenses). Add more pigments or more cells, and the vision becomes sharper. Each alteration is just a slight change from the one before, a minor improvement well within bounds of evolution’s toolkit, but over time these small adjustments led to intricate complexity.
In the Cambrian, eyes were all the rage. Arthropods were visual trendsetters, creating compound eyes by using the latter approach, that of bulging, then combining many little bulges together. One of the era’s top predators, Anomalocaris, had over 16,000 lenses! So many creatures arose with eyes during the Cambrian that Andrew Parker, a visiting member of the Zoology Department at the University of Oxford, believes that the development of vision was the driver behind the evolutionary explosion. His ‘Light-Switch’ hypothesis postulates that vision opened the doors for animal innovation, allowing rapid diversification in modes and mechanisms for a wide set of ecological traits. Even if eyes didn’t spur the Cambrian explosion, their development certainly irrevocably altered the course of evolution.
Our eyes, as well as those of octopuses and fish, took a different approach than those of the arthropods, putting photo receptors into a pit, thus creating what is referred to as a camera-style eye. In the fossil record, eyes seem to emerge from eyeless predecessors rapidly, in less than 5 million years. But is it really possible that an eye like ours arose so suddenly? Yes, say biologists Dan-E. Nilsson and Susanne Pelger. They calculated a pessimistic guess as to how long it would take for small changes – just 1% improvements in length, depth, etc per generation – to turn a flat eyespot into an eye like our own. Their conclusion? It would only take about 400,000 years – a geological instant.
But how does complexity arise in the first place? How did cells get photoreceptors, or any of the first steps towards innovations such as vision? Well, complexity can arise a number of ways.
Each and every one of our cells is a testament to the simplest way that complexity can arise: have one simple thing combine with a different one. The powerhouses of our cells, called mitochondria, are complex organelles that are thought to have arisen in a very simple way. Some time around 3 billion years ago, certain bacteria had figured out how to create energy using electrons from oxygen, thus becoming aerobic. Our ancient ancestors thought this was quite a neat trick, and, as single cells tend to do, they ate these much smaller energy-producing bacteria. But instead of digesting their meal, our ancestors allowed the bacteria to live inside them as an endosymbiont, and so the deal was struck: our ancestor provides the fuel for the chemical reactions that the bacteria perform, and the bacteria, in turn, produces ATP for both of them. Even today we can see evidence of this early agreement – mitochondria, unlike other organelles, have their own DNA, reproduce independently of the cell’s reproduction, and are enclosed in a double membrane (the bacterium’s original membrane and the membrane capsule used by our ancestor to engulf it). Over time the mitochondria lost other parts of their biology they didn’t need, like the ability to move around, blending into their new home as if they never lived on their own. The end result of all of this, of course, was a much more complex cell, with specialized intracellular compartments devoted to different functions: what we now refer to as a eukaryote.
Of course, while I focused this post on how complexity arose, it’s important to note that more complex doesn’t necessarily mean better. While we might notice the eye and marvel at its detail, success, from the viewpoint of an evolutionary lineage, isn’t about being the most elaborate. Evolution only leads to increases in complexity when complexity is beneficial to survival and reproduction. Indeed, simplicity has its perks: the more simple you are, the faster you can reproduce, and thus the more offspring you can have. Many bacteria live happy simple lives, produce billions of offspring, and continue to thrive, representatives of lineages that have survived billions of years. Even complex organisms may favor less complexity – parasites, for example, are known for their loss of unnecessary traits and even whole organ systems, keeping only what they need to get inside and survive in their host. Darwin referred to them as regressive for seemingly violating the unspoken rule that more complex arises from less complex, not the other way around. But by not making body parts they don’t need, parasites conserve energy, which they can invest in other efforts like reproduction.
When we look back in an attempt to grasp evolution, it may instead be the lack of complexity, not the rise of it, that is most intriguing.
Ratcliff, W. C., Denison, R. F., Borello, M., & Travisano, M. (2012). Experimental evolution of multicellularity. PNAS Early Edition, 1–6. doi:10.1073/pnas.1115323109
Schwab, I. R. (2012). Evolution’s Witness: How Eyes Evolved. Oxford University Press, 297 pp.
Parker, A. (2003). In the blink of an eye. Basic Books, 352 pp.
Nilsson, D.-E. & Pelger, S. (1994). A Pessimistic Estimate of the Time Required for an Eye to Evolve. Proceedings: Biological Sciences Vol. 256, No. 1345, pp. 53-58
Reijnders, L. (1975). The origin of mitochondria. Journal of Molecular Evolution Vol. 5, No. 3, pp. 167-176. DOI: 10.1007/BF01741239
Every plant and animal out there produces miRNAs. We, for example, are thought to produce thousands. These teeny-tiny snippets of RNA serve regulatory roles in our cells, attaching to bits of messenger RNA and causing changes in expression of different proteins. They are far from evil: indeed, miRNAs are necessary for cells to function properly.
Can miRNAs we eat alter our gene expression? Well, yes. That was the incredible scientific discovery made by the Chinese research team that was recently published in Cell Research. But to make the leap from ‘miRNAs we eat can alter gene expression’ to ‘GMOs are dangerous’ requires unbelievable gaps in understanding about GMOs and miRNAs.
First off, there’s no reason to think that the DNA being introduced into GMOs is going to produce more/different miRNAs than it did in the original organism. Ari’s claim that “new DNA can have dangerous implications far beyond the products it codes for” simply isn’t true because miRNAs are coded for. These small RNA fragments aren’t random or accidental – they are explicitly detailed within the genome. So a stretch of DNA that didn’t code any miRNAs before isn’t going to suddenly code for a ton of them when it’s placed in a different genome. If we’re worried about potential miRNA effects, we can screen genes we are considering transferring and determine if there is any chance they produce miRNAs before we shuffle around which organism they are in. Indeed, GMOs are tested genetically, to ensure that the target gene has incorporated properly and that the organism is producing the desired protein, and not unexpected products. Genetic modification is a very precise process, and there is no reason to think it would cause a sudden burst of miRNAs.
But perhaps more fundamentally, miRNAs are found in all kinds of life, including every single species that we currently eat. There’s no logical reason that a new miRNA being produced by a GM plant is going to be more dangerous than the multitude of miRNAs we ingest when we eat the non-GM version.
In fact, the potential side effects of non-GM food is, very explicitly, what the Chinese research team showed: that of the millions of miRNAs we eat every day, at least a few make it from our stomachs into our blood, and that a specific one from ordinary rice can change the expression of genes in mice. So if miRNAs are dangerous – guess what? – you’re already ingesting them every time you eat. And, to get a little gross, let’s be clear: when we eat something, we don’t just ingest the miRNAs from the species we intentionally eat. Did you know, for example, that foods you eat are allowed to contain mold, hair, insect parts, and even rat poop? All of those bits of organisms which we inadvertently eat have DNA, and – you guessed it! – miRNAs, too. If miRNAs are so dangerous, we would never have been able to eat anything previously alive in the first place.
But we can eat other organisms, and we will continue to, because, simply put, miRNAs aren’t that dangerous.
Perhaps what ticks me off most, though, is that Ari’s scaremongering overshadows the very real and interesting implications of the science he failed to cover. The notion that miRNAs may drive some of the interaction between us and our food is incredibly new and totally cool. As the authors write, their research suggests that “miRNAs may represent a novel class of universal modulators that play an important role in mediating animal-plant interactions at the molecular level. Like vitamins, minerals and other essential nutrients derived from food sources, plant miRNAs may serve as a novel functional component of food and make a critical contribution to maintaining and shaping animal body structure and function.”
What if some of the benefits of drinking wine aren’t from the antioxidants, but from the miRNAs present in grapes? What if we can produce beneficial miRNAs, and take them like we do vitamins? Or reduce the expression of harmful ones? Suddenly, we have been given a sneak peek at a whole new facet of nutrition science that we didn’t even know existed. The amazing implications of this research – not some ludicrous and tenuous connection to anti-GMO propaganda – should have been what The Atlantic highlighted. Instead, they made a fool of themselves by allowing Ari Levaux to expose just how poorly he understands genetics.
One of the toughest concepts to grasp about evolution is its lack of direction. Take the classic image of the evolution of man, from knuckle-walking ape to strong, smart hunter:
We view this as the natural progression of life. Truth is, there was no guarantee that some big brained primates in Africa would end up like we are now. It wasn’t inevitable that we grew taller, less hairy, and smarter than our relatives. And it certainly wasn’t guaranteed that single celled bacteria-like critters ended up joining forces into multicellular organisms, eventually leading to big brained primates!
Evolution isn’t predictable, and randomness is key in determining how things change. But that’s not the same as saying life evolves by chance. That’s because while the cause of evolution is random (mutations in our genes) the processes of evolution (selection) is not. It’s kind of like playing poker – the hand you receive is random, but the odds of you winning with it aren’t. And like poker, it’s about much more than just what you’re dealt. Outside factors – your friend’s ability to bluff you in your poker game, or changing environmental conditions in the game of life – also come into play. So while evolution isn’t random, it is a game of chance, and given how many species go extinct, it’s one where the house almost always wins.
Of course chance is important in evolution. Evolution occurs because nothing is perfect, not even the enzymes which replicate our DNA. All cells proliferate and divide, and to do so, they have to duplicate their genetic information each time. The enzymes which do this do their best to proof-read and ensure that they’re faithful to the original code, but they make mistakes. They put in a guanine instead of an adenine or a thymine, and suddenly, the gene is changed. Most of these changes are silent, and don’t affect the final protein that each gene encodes. But every once in awhile these changes have a bigger impact, subbing in different amino acids whose chemical properties alter the protein (usually for the worse, but not always).Or our cells make bigger mistakes – extra copies of entire genes or chromosomes, etc.
These genetic changes don’t anticipate an individual’s needs in any way. Giraffes didn’t “evolve” longer necks because they wanted to reach higher leaves. We didn’t “evolve” bigger brains to be better problem solvers, social creatures, or hunters. The changes themselves are random*. The mechanisms which influence their frequency in a population, however, aren’t. When a change allows you (a mutated animal) to survive and reproduce more than your peers, it’s likely to stay and spread through the population. This is selection, the mechanism that drives evolution. This can mean either natural selection (because it makes you run faster or do something to survive in your environment) or sexual selection (because even if it makes you less likely to survive, the chicks dig it). Either way the selection isn’t random: there’s a reason you got busier than your best friend and produced more offspring. But the mutation occurring in the first place – now that was luck of the draw.
Mistakes made by genetic machinery can lead to huge differences in organisms. Take flowering plants, for example. Flowering plants have a single gene that makes male and female parts of the flower. But in many species, this gene was accidentally duplicated about 120 million years ago. This gene has mutated and undergone selection, and has ended up modified in different species in very different ways. In rockcress (Arabidopsis), the extra copy now causes seed pods to shatter open. But it’s in snap dragons that we see how the smallest changes can have huge consequences. They, too, have two copies of the gene to make reproductive organs. But in these flowers, each copy fairly exclusively makes either male or female parts. This kind of male/female separation is the first step towards the sexes split into individual organisms, like we do. Why? It turns out that mutations causing the addition of a single amino acid in the final protein makes it so that one copy of the gene can only make male bits. That’s it. A single amino acid makes a gene male-only instead of both male and female.
Or, take something as specialized as flight. We like to think that flight evolved because some animals realized (in some sense of the word) the incredible advantage it would be to take to the air. But when you look at the evolution of flight, instead, it seems it evolved, in a sense, by accident. Take the masters of flight – birds – for example.
There are a few key alterations to bird bodies that make it so they can fly. The most obvious, of course, are their feathers. While feathers appear to be so ideally designed for flight, we are able to look back and realize that feathers didn’t start out that way. Through amazing fossil finds, we’re able to glimpse at how feathers arose, and it’s clear that at first, they were used for anything but airborne travel. These protofeathers were little more than hollow filaments, perhaps more akin to hairs, that may have been used in a similar fashion. More mutations occurred, and these filaments began to branch, join together. Indeed, as we might expect for a structure that is undergoing selection and change, there are dinosaurs with feather-like coverings of all kinds, showing that there was a lot of genetic experimentation and variety when it came to early feathers. Not all of these protofeathers were selected for, though, and in the end only one of these many forms ended up looking like the modern feather, thus giving a unique group of animals the chance to fly.
There’s a lot of variety in what scientists think these early feathers were used for, too. Modern birds use feathers for a variety of functions, including mate selection, thermoregulation and camouflage, all of which have been implicated in the evolution of feathers. There was no plan from the beginning, nor did feathers arise overnight to suddenly allow dinosaurs to fly. Instead, accumulations of mutations led to a structure that happened to give birds the chance to take to the air, even though that wasn’t its original use.
The same is true for flying insects. Back in the 19th century, when evolution was fledging as a science, St. George Jackson Mivart asked “What use is half a wing?” At the time he intended to humiliate the idea that wings could have developed without a creator. But studies on insects have shown that half a wing is actually quite useful, particularly for aquatic insects like stoneflies (close relatives of mayflies). Scientists experimentally chopped down the wings of stoneflies to see what happened, and it turned out that though they couldn’t fly, they could sail across the water much more quickly while using less energy to do so. Indeed, early insect wings may have functioned in gliding, only later allowing the creatures to take to the air. Birds can use half a wing, too – undeveloped wings help chicks run up steeper hills – so half a wing is quite a useful thing.
But what’s really key is that if you rewound time and took one of the ancestors of modern birds, a dino with proto-feathers, or a half-winged insect and placed it in the same environment with the same ecological pressures, its decedents wouldn’t necessarily fly.
That’s because if you do replay evolution, you never know what will happen. Recently, scientists have shown this experimentally in the lab with E. coli bacteria. They took a strain of E. coli and separated it into 12 identical petri dishes containing a novel food source that the bacteria could not digest, thus starting with 12 identical colonies in an environment with strong selective pressure. They grew them for some 50,000 generations. Every 500 generations, they froze some of the bacteria. Some 31,500 generations later, one of the twelve colonies developed the ability to feed off of the new nutrient, showing that despite the fact that all of them started the same, were maintained in the same conditions and exposed to the exact same pressures, developing the ability to metabolize the new nutrient was not a guarantee. But even more shocking was that when they replayed that colony’s history, they found that it didn’t always develop the ability, either. In fact, when replayed anywhere from the first to the 19,999th generation, no luck. Some change occurring in the 20,000 generation or so – a good 11,500 generations before they were able to metabolize the new nutrient – had to be in place for the colony to gain its advantageous ability later on.
There’s two reasons for this. The first is that the mutations themselves are random, and the odds of the same mutations occurring in the same order are slim. But there’s another reason we can’t predict evolution: genetic alterations don’t have to be ‘good’ (from a selection standpoint) to stick around, because selection isn’t the only evolutionary mechanism in play. Yes, selection is a big one, but there can be changes in the frequency of a given mutation in a population without selection, too. Genetic drift occurs when events change the gene frequencies in a population for no reason whatsoever. A massive hurricane just happens to wipe out the vast majority of a kind of lizard, for example, leaving the one weird colored male to mate with all the girls. Later, that color may end up being a good thing and allowing the lizards to blend in a new habitat, or it may make them more vulnerable to predators. Genetic drift doesn’t care one bit.
Every mutation is a gamble. Even the smallest mutations – a change of a single nucleotide, called a point mutation – matter. They can lead to terrible diseases in people like sickle cell anemia and cystic fibrosis. Of course, point mutations also lead to antibiotic resistance in bacteria.
What does the role of chance mean for our species? Well, it has to do with how well we can adapt to the changing world. Since we can’t force our bodies to mutate beneficial adaptations (no matter what Marvel tells you), we rely on chance to help our species continue to evolve. And believe me, we as a species need to continue to evolve. Our bodies store fat because in the past, food was sporadic, and storing fat was the best solution to surviving periods of starvation. But now that trait has led to an epidemic of obesity, and related diseases like diabetes. As diseases evolve, too, our treatments fail, leaving us vulnerable to mass casualties on the scale of the bubonic plague. We may very well be on the cusp of the end of the age of man, if random mutations can’t solve the problems presented by our rapidly changing environment. What is the likelihood that man will continue to dominate, proliferate, and stick around when other species go extinct? Well, like any game of chance, you have to look at the odds:
99.99% of all the species that have ever existed are now extinct.
But then again – maybe our species is feeling lucky.
* If you want to get into more detail, actually, mutations aren’t completely random. They, too, are governed by natural laws – our machinery is more likely to sub an adenine for a guanine than for a thymine, for example. Certain sections are more likely to be invaded by transposons… etc. But from the viewpoint of selection, these changes are random – as in, a mutation’s potential selective advantage or disadvantage has no effect on how likely it is to occur.
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Perrichot, V., Marion, L., Neraudeau, D., Vullo, R., & Tafforeau, P. (2008). The early evolution of feathers: fossil evidence from Cretaceous amber of France Proceedings of the Royal Society B: Biological Sciences, 275 (1639), 1197-1202 DOI: 10.1098/rspb.2008.0003
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It’s 8:09 PM here in Hawaii – hours until we say goodbye to 2011 and hello to 2012. We’re one of the last to experience the ushering in of the new year, and thus I have had a lot of time to think about my new year’s post. I wanted to sum up 2011 in a grandiose manner. More than just a tally of the year’s accomplishments, I wanted this post to be a resonating last word. But every time I tried to sit down and write, I found myself blocked. That’s the funny thing about writing – the more complete, profound and impressive you want your words to be, the more totally inept you become at writing them.
Well, here I am anyway. I’ve spent the past few days reflecting on the past year, and thinking about my hopes for the next one. In accordance with proper US traditions, I feel obliged to write down some resolutions. It’s probably a silly endeavor – the science has found that new year’s resolutions are indifferent at best. Still, it can’t hurt to try. So here are my hopes and goals for 2012:
Take at least 10 minutes every week to reflect on the positive. No matter how bad things are, or how stressful life might get, studies have shown that taking time to focus on what you’re thankful for can improve your health and happiness. So I resolve to take that time and truly contemplate the things in my life that make me happy.
Read. I have a number of books that have been gathering dust on my bookshelf for the past few months because I ‘don’t have time’ or ‘have so many more important things to do.’ Well screw it. I love reading – it’s my personal escape from the rest of the world. So, I resolve to read more. A lot more.
There’s this great song by Sara Bareilles, and in it, she has this line that always hits me: “I’m not the girl that I intend to be. But I dare you darlin’, just you wait and see.” I think we all are like that to some extent; we have all these high hopes or ideals that we strive to live up to, and end up falling short because we simply don’t care enough to push for it. Well, I resolve to be the person I intend to be, at least as much as I can. Nothing extraordinary, just the best version of me that I can be.
So there you have it. My three new year’s resolutions. What about you? What are your hopes for the new year?