Evolution – Page 8 – Science Sushi

Evolution: The Rise of Complexity

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.

Evolution of Snowflake Yeast — Images of the snowflake-like pattern that arose in all of the experimental cell cultures from Ratcliff et al. 2012

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.

Cambrian Arthropod Eyes — Fossilized compound eyes from Cambrian arthropods (Lee et al. 2011)

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.

endosymbiosis_c_la_784 — An illustration of the endosymbiont hypothesis

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.

Complexity can arise within a cell, too, because our molecular machinery makes mistakes. On occasion, it duplicates sections of DNA, entire genes, and even whole chromosomes, and these small changes to our genetic material can have dramatic effects. We saw how mutations can lead to a wide variety of phenotypic traits when we looked at how artificial selection has shaped dogs. These molecular accidents can even lead to complete innovation, like the various adaptations of flowering plants that I talked about in my last Evolution post. And as these innovations accumulate, species diverge, losing the ability to reproduce with each other and filling new roles in the ecosystem. While the creatures we know now might seem unfathomably intricate, they are the product of billions of years of slight variations accumulating.

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.

Other Posts in the Evolution Series:

References

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

The Very Real Scaremongering of Ari Levaux

Recently, food columnist Ari Levaux wrote what can only be described as a completely unscientific article in The Atlantic claiming that microRNAs (miRNAs) are a “very real danger of GMOs.” I won’t go point by point through the horrendous inaccuracies in his piece, as Emily Willingham has more than hacked them to bits. But I do want to make a short comment on this idea that miRNAs are dangerous, and thus something we should worry about when it comes to what we eat.

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.

Evolution: A Game of Chance | Observations

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 19^th 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.

Originally posted Nov 1st, 2010.

References:

Airoldi, C., Bergonzi, S., & Davies, B. (2010). Single amino acid change alters the ability to specify male or female organ identity Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.1009050107

XU Xing, & GUO Yu (2009). THE ORIGIN AND EARLY EVOLUTION OF FEATHERS: INSIGHTS

FROM RECENT PALEONTOLOGICAL AND NEONTOLOGICAL DATA Verbrata PalAsiatica, 47 (4), 311-329

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

Marden, J., & Kramer, M. (1994). Surface-Skimming Stoneflies: A Possible Intermediate Stage in Insect Flight Evolution Science, 266 (5184), 427-430 DOI: 10.1126/science.266.5184.427

DIAL, K., RANDALL, R., & DIAL, T. (2006). What Use Is Half a Wing in the Ecology and Evolution of Birds? BioScience, 56 (5) DOI: 10.1641/0006-3568(2006)056[0437:WUIHAW]2.0.CO;2

Blount, Z., Borland, C., & Lenski, R. (2008). Inaugural Article: Historical contingency and the evolution of a key innovation in an experimental population of Escherichia coli Proceedings of the National Academy of Sciences, 105 (23), 7899-7906 DOI: 10.1073/pnas.0803151105

Evolution: Watching Speciation Occur | Observations

This is a repost from April 24^th, 2010. Watching Speciation Occur is the second in my Evolution series which started with The Curious Case of Dogs

We saw that the littlest differences can lead to dramatic variations when we looked at the wide variety in dogs. But despite their differences, all breeds of dogs are still the same species as each other and their ancestor. How do species split? What causes speciation? And what evidence do we have that speciation has ever occurred?

Critics of evolution often fall back on the maxim that no one has ever seen one species split into two. While that’s clearly a straw man, because most speciation takes far longer than our lifespan to occur, it’s also not true. We have seen species split, and we continue to see species diverging every day.

For example, there were the two new species of American goatsbeards (or salsifies, genus Tragopogon) that sprung into existence in the past century. In the early 1900s, three species of these wildflowers – the western salsify (T. dubius), the meadow salsify (T. pratensis), and the oyster plant (T. porrifolius) – were introduced to the United States from Europe. As their populations expanded, the species interacted, often producing sterile hybrids. But by the 1950s, scientists realized that there were two new variations of goatsbeard growing. While they looked like hybrids, they weren’t sterile. They were perfectly capable of reproducing with their own kind but not with any of the original three species – the classic definition of a new species.

How did this happen? It turns out that the parental plants made mistakes when they created their gametes (analogous to our sperm and eggs). Instead of making gametes with only one copy of each chromosome, they created ones with two or more, a state called polyploidy. Two polyploid gametes from different species, each with double the genetic information they were supposed to have, fused, and created a tetraploid: an creature with 4 sets of chromosomes. Because of the difference in chromosome number, the tetrapoid couldn’t mate with either of its parent species, but it wasn’t prevented from reproducing with fellow accidents.

This process, known as Hybrid Speciation, has been documented a number of times in different plants. But plants aren’t the only ones speciating through hybridization: Heliconius butterflies, too, have split in a similar way.

It doesn’t take a mass of mutations accumulating over generations to create a different species – all it takes is some event that reproductively isolates one group of individuals from another. This can happen very rapidly, in cases like these of polyploidy. A single mutation can be enough. Or it can happen at a much, much slower pace. This is the speciation that evolution is known for – the gradual changes over time that separate species.

But just because we can’t see all speciation events from start to finish doesn’t mean we can’t see species splitting. If the theory of evolution is true, we would expect to find species in various stages of separation all over the globe. There would be ones that have just begun to split, showing reproductive isolation, and those that might still look like one species but haven’t interbred for thousands of years. Indeed, that is exactly what we find.

The apple maggot fly, Rhagoletis pomonella is a prime example of a species just beginning to diverge. These flies are native to the United States, and up until the discovery of the Americas by Europeans, fed solely on hawthorns. But with the arrival of new people came a new potential food source to its habitat: apples. At first, the flies ignored the tasty treats. But over time, some flies realized they could eat the apples, too, and began switching trees. While alone this doesn’t explain why the flies would speciate, a curious quirk of their biology does: apple maggot flies mate on the tree they’re born on. As a few flies jumped trees, they cut themselves off from the rest of their species, even though they were but a few feet away. When geneticists took a closer look in the late 20th century, they found that the two types – those that feed on apples and those that feed on hawthorns – have different allele frequencies. Indeed, right under our noses, Rhagoletis pomonella began the long journey of speciation.

As we would expect, other animals are much further along in the process – although we don’t always realize it until we look at their genes.

Orcas (Orcinus orca), better known as killer whales, all look fairly similar. They’re big dolphins with black and white patches that hunt in packs and perform neat tricks at Sea World. But for several decades now, marine mammalogists have thought that there was more to the story. Behavioral studies have revealed that different groups of orcas have different behavioral traits. They feed on different animals, act differently, and even talk differently. But without a way to follow the whales underwater to see who they mate with, the scientists couldn’t be sure if the different whale cultures were simply quirks passed on from generation to generation or a hint at much more.

Now, geneticists have done what the behavioral researchers could not. They looked at how the whales breed. When they looked at the entire mitochondrial genome from 139 different whales throughout the globe, they found dramatic differences. These data suggested there are indeed at least three different species of killer whale. Phylogenetic analysis indicated that the different species of orca have been separated for 150,000 to 700,000 years.

Why did the orcas split? The truth is, we don’t know. Perhaps it was a side effect of modifications for hunting different prey sources, or perhaps there was some kind of physical barrier between populations that has since disappeared. All we know is that while we were busy painting cave walls, something caused groups of orcas to split, creating multiple species.

There are many different reasons why species diverge. The easiest, and most obvious, is some kind of physical barrier – a phenomenon called Allopatric Speciation. If you look at fish species in the Gulf of Mexico and off the coast of California, you’ll find there are a lot of similarities between them. Indeed, some of the species look almost identical. Scientists have looked at their genes, and species on either side of that thin land bridge are more closely related to each other than they are to other species, even ones in their area. What happened is that a long time ago, the continents of North and South America were separated, and the oceans were connected. When the two land masses merged, populations of species were isolated on either side. Over time, these fish have diverged enough to be separate species.

Species can split without such clear boundaries, too. When species diverge like the apple maggot flies – without a complete, physical barrier – it’s called Sympatric Speciation. Sympatric speciation can occur for all kinds of reasons. All it takes is something that makes one group have less sex with another.

For one species of Monarch flycatchers (Monarcha castaneiventris), it was all about looks. These little insectivores live on Solomon Islands, east of Papua New Guinea. At some point, a small group of them developed a single amino acid mutation in the gene for a protein called melanin, which dictates the bird’s color pattern. Some flycatchers are all black, while others have chestnut colored bellies. Even though the two groups are perfectly capable of producing viable offspring, they don’t mix in the wild. Researchers found that the birds already see the other group as a different species. The males, which are fiercely territorial, don’t react when a differently colored male enters their turf. Like the apple maggot flies, the flycatchers are no longer interbreeding, and have thus taken the first step towards becoming two different species.

These might seem like little changes, but remember, as we learned with dogs, little changes can add up. Because they’re not interbreeding, these different groups will accumulate even more differences over time. As they do, they will start to look less and less alike. The resultant animals will be like the species we clearly see today. Perhaps some will adapt to a lifestyle entirely different from their sister species – the orcas, for example, may diverge dramatically as small changes allow them to be better suited to their unique prey types. Others may stay fairly similar, even hard to tell apart, like various species of squirrels are today.

The point is that all kinds of creatures, from the smallest insects to the largest mammals, are undergoing speciation right now. We have watched species split, and we continue to see them diverge. Speciation is occurring all around us. Evolution didn’t just happen in the past; it’s happening right now, and will continue on long after we stop looking for it.

Soltis, D., & Soltis, P. (1989). Allopolyploid Speciation in Tragopogon: Insights from Chloroplast DNA American Journal of Botany, 76 (8) DOI: 10.2307/2444824
McPheron, B., Smith, D., & Berlocher, S. (1988). Genetic differences between host races of Rhagoletis pomonella Nature, 336 (6194), 64-66 DOI: 10.1038/336064a0
Uy, J., Moyle, R., Filardi, C., & Cheviron, Z. (2009). Difference in Plumage Color Used in Species Recognition between Incipient Species Is Linked to a Single Amino Acid Substitution in the Melanocortin?1 Receptor The American Naturalist, 174 (2), 244-254 DOI: 10.1086/600084
Phillip A Morin1, Frederick I Archer, Andrew D Foote, Julie Vilstrup, Eric E Allen, Paul Wade, John Durban, Kim Parsons, Robert Pitman, Lewyn Li, Pascal Bouffard, Sandra C Abel Nielsen, Morten Rasmussen, Eske Willerslev, M. Thomas P Gilbert, & Timothy Harkins (2010). Complete mitochondrial genome phylogeographic analysis of killer whales (Orcinus orca) indicates multiple species Genome Research

Image Credits:

Salsify plate showing two new species from the New Zealand Plant Radiation Network (taken from Ownbey, 1950 in which the species were described)

Flycatchers image by Robert Boyle, as featured on Science Now

Science Bloggers Compete for $10,000

Last year, I entered this $10,000 blogging scholarship on a whim. After all, why not? $10,000 is a lot of money, money that as a poor grad student, I could definitely use. I remember I was so excited when I saw that I’d made it into the list of finalists – the only science blogger in the running. I was even more excited, and a little amazed, when I won, thanks to the incredible support of the science blogging community.

This year, I’m thrilled to see that there are a whopping total of six science bloggers in the race. I’m glad I won last year, because I’d hate to have to compete with the talent in the running now! I encourage you to visit each and every one of the six blogs I’m about to link to, as well as the other finalists. These students need votes to win the scholarship, which means they need your help. All you have to do is follow this link and vote for the one you think deserves to win the most. I also want to encourage you to pass this along and get your friends, family and social networks to do the same.

So, without further ado, here are the science finalists:

Biology Blogs

Yes, I’m listing the bio blogs first. I’m biased. Given my career field of choice, it’s no wonder that these blogs have a special place in my heart. Bio blogs are a whopping 15% of the entries this year – way to go, biology lovers! Here are the three bio-themed blogs, in order of appearance in the overall list:

David Shiffman: Southern Fried Science

Ahoy, matey! If you’ve never sailed over to Southern Fried Science before, you don’t know what you’re missing. This marine-themed blog is the perfect blend of science and saltiness. David’s coblogger, Andrew, just posted a nice list of some of David’s best posts, which I highly recommend reading.

Heather Cohen: Escaping Anergy

It’s not easy to make immunology engaging and interesting, but Heather does a fantastic job of it. She clearly has a passion for what she does, and loves to share it with others. She hopes that her blog will help connect the general public to a field that is often overhyped and misinterpreted – and I’d say she’s off to a damn good start.

Jacquelyn Gill: Contemplative Mammoth

I grew up reading prehistorical fiction like The Clan of the Cave Bear. As a child, I wished more than anything I could travel back and time and walk among mammoths. Well, Jacquelyn does, every day. Her job as a paleoecologist is to use clues in the fossil record and from the world around us to recreate and study the past. Her blog brings readers back with her, exploring the science which lets us learn about the world as it once was as well as what it’s like to be a graduate student now, studing animals long since extinct.

Physics & Astronomy

I saw this great cartoon the other day, which definitely applies here. I guess if you can’t study the life on this planet, studying the rest of the universe is not a bad compromise. Two finalists manage to make the non-life sciences fun to read:

Philip Tanedo: Quantum Diaries

A little confession: I almost became a physicist. At least, I listed myself as a physics major when I started undergrad. In the end, I couldn’t hack it as a theoretical physicist, so I have a lot of respect for anyone who can make the Higgs boson into something I actually care about. Philip (or Flip) has a knack for turning some of the most complex topics out there into fun, entertaining reads.

Ray Sanders: Dear Astronomer.com

Ray wants to be sure that no astronomy question goes unanswered. If you have a question about our universe, he’ll try to answer it. He started his blog with the express purpose of acting as resource, complete with a good helping of “cheeky shenanigans to help make Astronomy fun and entertaining.”

Data Analysis

What is science without good data analysis? Sure, the last blog on my list isn’t *exactly* a science blog, but he sneaks in here because anyone who finds talking about data to be a fun hobby is a scientist at heart.

Kevin Flora: EdMatics

Kevin is a perfect example of why this contest is so great. I’d never heard of EdMantics before this, but when I checked out his blog, I was stunned. Who thought data could be so interesting? Kevin writes about presenting and analyzing data as if it is an art form – which, frankly, it is. He gets major kudos from me for turning most scientists’ least favorite part of the job into something beautiful.

Evolution: The Curious Case of Dogs | Observations

This is the first in a series of post of mine about Evolution that I started posting in January of 2010. I’ll be reposting the series over the next two months, culminating in a brand new post for the set in Jan 2012! I’m excited. You know you’re excited. Enjoy!

Man’s best friend is much more than a household companion – for centuries, artificial selection in dogs has made them prime examples of the possibilities of evolution. A century and a half ago, Charles Darwin recognized how the incredibly diverse dogs supported his revolutionary theory in his famous book On The Origin Of Species. At the time, he believed that dogs varied so much that they must have been domesticated from multiple canine species. Even still, he speculated that:

if… it could be shown that the greyhound, bloodhound, terrier, spaniel and bull-dog, which we all know propagate their kind truly, were the offspring of any single species, then such facts would have great weight in making us doubt about the immutability of the many closely allied natural species

If only Darwin knew what we know now, that indeed, all dogs did descend from one species!

While humans have been breeding dogs for over ten thousand years, it was until recently that strict standards and the emphasis on “purebreds” has led to over 400 different breeds that are some of the best examples of the power of selection. Those that doubt whether small variations in traits can lead to large levels of diversity clearly haven’t compared a Pug to a Great Dane – I mean, just look at them compared to their ancestor:

We’ve turned a fine-tuned hunting animal, the wolf, into a wide variety of creatures, from the wolf-looking shepherds to the bizarre toy breeds. Before domestication, dog’s life was tough. But when people pulled specific wolves out of their packs and began breeding them, we changed everything. There were some traits that made this easy – the social structure of wolves, for example, made them predisposed to belonging to a community. Still, we opened up a number of genetic traits and allowed them to express variety that would have been fatal in the wild. We not only allowed these traits to persist, we encouraged them. We picked dogs that were less aggressive or looked unique. And in doing so, we spurred on rapid diversification and evolution in an unbelievable way.

Take their skulls, for example. Like other members of the order Carnivora, dog’s skulls have a few distinctive characteristics: relatively large brains and a larger-than-normal structure called a zygomatic arch which allows for bite power and chewing. But years of hand-picked puppies has led to an amazing amount of skull diversity in dogs. A study recently compared the positions of 50 recognizable points on the skulls of dogs and compared them to each other and other members of the order Carnivora. They found that there was as much variety in the shape of the skulls of dogs as in the entire rest of the order, and the extremes were further apart. What does that mean, exactly? It means that the differences between the skulls of that Pug and Great Dane I mentioned before (on R) are greater than the differences between the skulls of a weasel and a walrus. Much of this variation is outside the range of the rest of the order, meaning dogs’ skull shapes are entirely unique. In just a few centuries, our choices have created unbelievable variety in the heads of dogs – more than 60 million years has created in the rest of the carnivores.

The amazing diversity of dogs is a testimonial to the possibilities of selection. And it’s not just their skulls that vary. A joint venture between the University of Washington and the Veterinary School at UC Davis mapped the variation in the genomes of a mere 10 different breeds of dogs. They found that at least 155 different regions of the dog’s genome show evidence of strong artificial selection. Each region contained, on average, 11 genes, so it’s harder to identify exactly what about each area was under the most selection, though there were clues. About 2/3 of these areas contain genes that were uniquely modified in only one or two breeds, suggesting they contain genes that are highly breed-restricted like the skin wrinkling in the Shar-Pei. Another 16 had variations in 5 or more breeds, suggesting they encode for traits that are altered in every breed, like coat and size.

While we usually think of evolution as a slow and gradual process, dogs reveal that incredible amounts of diversity can arise very quickly, especially when selective pressures are very, very strong. It’s not hard to see how selection could lead to the differentiation of species – just look at the breeds of dogs that exist today. There’s a reason that you don’t see many Chihuahua/Saint Bernard mixes: while it’s entirely possible for their genetics to mix, it’s just physically difficult for these two breeds to actually do it. Just imagine what a poor Chihuahua female would have to endure to give birth to such a mix, or how hard it would be for male Chihuahua to mount a female Saint Bernard. Indeed, dogs are well on their way to speciation.

Of course, it’s at this point that I have to mention that while I have talked about “dogs” this entire time, they’re not actually a different species. Wolves are Canis lupus, while dogs are merely a subspecies of wolves, Canis lupus familiaris. Despite centuries of selective breeding and the vast array of physical differences, dogs are still able to breed with their ancestors.

When you take away the selective breeding done by humans, a number of these unique traits disappear. But feral dogs don’t just become wolves again – their behaviors and even looks depend greatly on the ecological pressures that surround them. Our centuries of selective breeding have opened a wide variety of traits, both physical and behavioral, that may help a stray dog survive and breed.

A good example of what happens to dogs when people are taken out of the picture can be found in Russia’s capital city. Feral dogs have been running around Moscow for at least 150 years. These aren’t just lost pets that band together – these dogs been on their own for awhile, and indeed, any poor, abandoned domesticated canine will meet an unfortunate fate at the hands of these territorial streetwalkers. Moscow’s dogs have lost traits like spotted coloration, wagging tails and friendliness that distinguish domesticated dogs from wolves – but they haven’t become them. The struggle to survive is tough for a stray, and only an estimated 3% ever breed. This strong selective pressure has led them to evolve into four distinct behavioral types, according to biologist Andrei Poyarkov who has studied the dogs for the past 30 years. There are guard dogs, who follow around security personnel, treating them as the alpha leaders of their packs. Others, called scavengers, have evolved completely different behaviors, preferring to roam the city for garbage instead of interacting with people. The most wolf-like dogs are referred to as wild dogs, and they hunt whatever they can find including cats and mice.

But the last group of Moscow’s dogs is by far the most amazing. They are the beggars, for obvious reasons. In these packs, the alpha isn’t the best hunter or strongest, it’s the smartest. The most impressive beggars, however, get their own title: ‘metro dogs’. They rely on scraps of food from the daily commuters who travel the public transportation system. To do so, the dogs have learned to navigate the subway. They know stops by name, and integrate a number of specific stations into their territories.

This dramatic shift from the survival of the fittest to the survival of the smartest has changed how Moscow’s dogs interact with humans and with each other. Beggars are rarely hit by cars, as they have learned to cross the streets when people do. They’ve even been seen waiting for a green light when no pedestrians are crossing, suggesting that they have actually learned to recognize the green walking man image of the crosswalk signal. Also, there are fewer “pack wars” that once were commonplace between Moscow’s stray canines, some of which used to last for months. However, they remain vigilant against the wild dogs and wolves that live on the outskirts of the city – rarely, if ever, are they permitted into Moscow. When politicians thought to remove the dogs, their use as a buffer against these animals was cited as a strong reason not to disturb them.

Moscow’s exemplary dogs show how different traits help dogs adapt to different ecological niches – whether it be brute strength for hunting in the truly feral wild dogs or intelligence in the almost-domesticated beggars. Some wonder if the strong selection for intellect will make Moscow’s metro dogs into another species all together, if left to their own devices.

Dogs make it easy to understand and demonstrate the core principles of evolution – variation and selection – and how they can make such a dramatic impact on an animal. It’s no wonder that Darwin took cues from domesticated animals when formulating his theory of evolution. However, there’s still a lot to learn about the processes that have shaped our best friends, and what future lies for them. How much time will it take to completely separate dogs from wolves, into their own species? What areas of the genome are key to doing so? In studying dogs and wolves, we may gain insight into how speciation occurs and when a threshold of change is met for it to do so. Seeing how much change has occurred already makes you wonder what surprises our canine companions still have in store for us as they, and we, continue to evolve together over the next ten thousand years.

Citations:

Drake, A., & Klingenberg, C. (2010). Large Scale Diversification of Skull Shape in Domestic Dogs: Disparity and Modularity The American Naturalist DOI: 10.1086/650372

Akey, J., Ruhe, A., Akey, D., Wong, A., Connelly, C., Madeoy, J., Nicholas, T., & Neff, M. (2010). Tracking footprints of artificial selection in the dog genome Proceedings of the National Academy of Sciences, 107 (3), 1160-1165 DOI: 10.1073/pnas.0909918107

Poyarkov, A.D., Vereshchagin, A.O., Goryachev, G.S., et al., Census and Population Parameters of Stray Dogs in Moscow, Zhivotnye v gorode: Mat-ly nauchno-prakt. konf. (Proc. Scientific and Practical Conf. Animals in the City ), Moscow, 2000, pp. 84 87.

Vereshchagin, A.O., Poyarkov, A.D., Rusov, P.V., et al., Census of Free-Ranging and Stray Animals (Dogs) in the Coty of Moscow in 2006, Problemy issledovanii domashnei sobaki: Mat-ly soveshch (Proc. Conf. on Problems in Studies on the Domestic Dog), Moscow, 2006, pp. 95 114.

Time – and brain chemistry – heal all wounds

I know I’m not physically hurt. Though it feels like I’ve been kicked in the stomach with steel-toed boots, my abdomen isn’t bruised. Spiking cortisol levels are causing my muscles to tense and diverting blood away from my gut, leading to this twisting, gnawing agony that I cannot stop thinking about. I can’t stop crying. I can’t move. I just stare at the ceiling, wondering when, if ever, this pain is going to go away.

It doesn’t matter that my injuries are emotional. The term heartache isn’t a metaphor: emotional wounds literally hurt. The exact same parts of the brain that light up when we’re in physical pain go haywire when we experience rejection. As far as our neurons are concerned, emotional distress is physical trauma.

Evolutionary biologists would say that it’s not surprising that our emotions have hijacked the pain system. As social creatures, mammals are dependent from birth upon others. We must forge and maintain relationships to survive and pass on our genes. Pain is a strong motivator; it is the primary way for our bodies tell us that something is wrong and needs to be fixed. Our intense aversion to pain causes us to instantly change behavior to ensure we don’t hurt anymore. Since the need to maintain social bonds is crucial to mammalian survival, experiencing pain when they are threatened is an adaptive way to prevent the potential danger of being alone.

Of course, being able to evolutionarily rationalize this feeling doesn’t make it go away.

I lie flattened, like the weight of his words has literally crushed me. I need to do something, anything to lessen this ache. The thought crosses my mind to self medicate, but I quickly decide against that. Mild analgesics like ibuprofen would be useless, as they act peripherally, targeting the pain nerves which send signals to the brain. In this case, it is my brain that is causing the pain. I would have to take something different, like an opioid, which depresses the central nervous system and thus inhibits the brain’s ability to feel. Tempting as that might be, painkillers are an easy – and dangerous – way out. No, I need to deal with this some other way.

Slowly, I sit up and grab the guitar at the foot of my bed.

Where music comes from, or even why we like and create music, is still a mystery. What we do know is that it has a powerful effect on our brains. Music evokes strong emotions and changes how we perceive the world around us. Simply listening to music causes the release of dopamine, a neurotransmitter linked to the brain’s reward system and feelings of happiness. But even more impressive is its effect on pain. Multiple studies have shown that listening to music alters our perception of painful stimuli and strengthens feelings of control. People are able to tolerate pain for longer periods of time when listening to music, and will even rate the severity of the sensation as lower, suggesting that something so simple as a melody has a direct effect on our neural pathways.

So, too, does self expression. Expressive writing about traumatic, stressful or emotional events is more than just a way to let out emotion – college students told to write about their most upsetting moments, for example, were found to be in remarkably better health four months later than their counterparts who wrote on frivolous topics. These positive results of self-expression are amplified when the product is shared with others. While negative emotions may have commandeered our pain response, art has tapped into the neurochemical pathways of happiness and healing.

So, I begin to write. At first, it is just a jumble of chords and words, haphazardly strung together. But, slowly, I edit and rewrite, weaving my emotions into lyrics. I play it over and over, honing the phrasing, perfecting the sound. Eventually, it begins to resemble a song:

(lyrics)

The rush of dopamine loosens the knot in my stomach ever so slightly. For now, the agony is dulled. Still, I can’t help but think that I’m never going to really feel better – that the memory of this moment will be seared into my brain, and a mental scar will always be there, torturing me with this intense feeling of loss.

Scientifically, I know I’m wrong. As I close my eyes, I am comforted by the thought that the human brain, though capable of processing and storing ridiculous amounts of information, is flawed. The permanence of memory is an illusion. My memory of this moment will weaken over time. It will be altered by future experiences, until what I envision when I try to recall it will be only a faint reflection of what I actually feel. Eventually, this pain won’t overwhelm me, and I will finally be able to let go.

A Moral Gene?

If our moral psychology is a Darwinian adaptation, what does that say about human nature? About social policy, which always presupposes something about human nature? About morality itself?

– Steven Pinker

Morality is often considered to be the domain of philosophers, not biologists. But scientists have often wondered what role our genomes play in directing our moral compass. Today, a paper was published in the open access journal PLoS ONE which found moral decision making was influenced by different forms of a single gene.

Picture yourself standing at branching train tracks with a unstoppable train barreling towards you. On one side, an evil villain has tied five people, while on the other, he has tied only one. You’ve got the switch in your hands which chooses which track the train goes down. Do you feel it’s morally acceptable to choose to kill the one instead of the five?

The scenario above is an example of foreseen harm. When such harm is unintentional, like in the train situation, most people are willing to go with Spock and say that the needs of the many outweigh the needs of the few. But previous research has found that people taking a particular group of antidepressants called selective serotonin reuptake inhibitors (SSRIs) were different – overall, they were less willing to say that killing the one person is morally justified, even if it’s unavoidable.

Serotonin is a chemical released at the junctions between nerves as a part of signaling in the brain. Since lower levels of serotonin are linked to sadness and depression, it is thought that by preventing the reuptake of serotonin, SSRIs fake higher overall serotonin levels and thus boost happy feelings.

But the connection between SSRIs and morality got Abigail Marsh and her colleagues from Georgetown University and the National Institutes of Health thinking. They knew that natural variation in serotonin reuptake ability exists in the population because of alterations in the promoter for one of the serotonin transmitter genes. People with the long form of the promoter (L) have normal levels of reuptake, while those with a truncated version (S) have reduced serotonin reuptake, similar to taking an SSRI. The researchers wondered if this natural variation influenced moral decision making in the same way that treatment with an SSRI does.

So, they took 65 healthy volunteers and tested their genes to see what versions of the promotor they had. Overall, 22 had two copies of the long form of the gene (LL), 30 had one of each (SL), and 13 had two copies of the short form of the gene (SS). They then asked these individuals to rate the overall morality of a variety of scenarios, including ones like the one above where one person is unintentionally harmed to save five others.

The results were clear: although the three groups showed no differences when presented with morally neutral scenarios or those where harm is intentionally caused to an individual, there were significant differences between groups when it came to scenarios of foreseen harm. Those with the long form of the promoter were much more willing to approve of harming one person to protect five. They felt that doing so was the better moral choice:

Those with the short form of the gene, however, felt that harming the one was morally neutral.

“I think this study is useful in helping to point out that maybe the way people arrive at their moral intuitions is just different for different people, in ways that are very deeply rooted,” says Marsh, the lead author, in a press release. Indeed, moral decision making may be as deeply rooted as it can be – that is, in our genomes.

Of course, as the quote from Steven Pinker at the beginning alluded, this kind of result leads to bigger questions. How has natural selection shaped what we think is right and wrong? How much of our moral code is influenced by our genes? And what does this say about the nature of morality itself?

Research: Marsh, A., Crowe, S., Yu, H., Gorodetsky, E., Goldman, D., & Blair, R. (2011). Serotonin Transporter Genotype (5-HTTLPR) Predicts Utilitarian Moral Judgments PLoS ONE, 6 (10) DOI: 10.1371/journal.pone.0025148

Observations: Why do women cry? Obviously, it’s so they don’t get laid.

This week, a paper came out looking at testosterone levels in fathers. A whirlwind of poor journalism followed, which was beautifully smacked down by William Saletan over at Slate (aslo: see this great post on the topic by our very own Kate Clancy). But it reminded me of a similar kerfluffle that occurred this past January over a paper on the effects of sniffing tears. This was my post from Jan 8^th on that paper and the media surrounding it, which just so happens to look at the meaning of lowered testosterone levels in terms of evolution.

I don’t think Brian Alexander is a bad guy or a misogynist. He writes the Sexploration column for MSNBC, so sure, his job is all about selling sex stories to the public. He even wrote a book about American sexuality. But I don’t personally think he has a burning hatred for women, or views them as objects placed on this Earth for the sexual satisfaction of men. However, I very easily could, given how he chose to report on a recent study published in Science about men’s physiological responses to the chemicals present in women’s tears.

The headline alone was enough to make me gag — “Stop the waterworks, ladies. Crying chicks aren’t sexy.” The sarcastic bitch in me just couldn’t help but think Why THANK YOU Brian! I’ve been going about this all wrong. When I want to get some from my honey, I focus all my thoughts on my dead dog or my great grandma and cry as hard as I can. No WONDER it isn’t working!

I didn’t even want to read the rest of the article.

But I did.

It doesn’t get better.

Alexander’s reporting of the actual science was quick and simplistic, and couched in sexist commentary (like how powerful women’s tears are as manipulative devices). And to finish things off, he clearly states what he found to be the most important find of the study:

“Bottom line, ladies? If you’re looking for arousal, don’t turn on the waterworks.”

It’s no wonder that the general public sometimes questions whether science is important. If that was truly the aim of this paper, I’d be concerned, too!

Of course, Brian Alexander missed the point. This paper wasn’t published as a part of a women’s how-to guide for getting laid. Instead, the authors sought to determine if the chemicals present in human tears might serve as chemosignals like they do for other animals — and they got some pretty interesting results.

In many species, chemical signals run rampant. Scents, pheromones, and other chemical cues are deliberately and unconsciously given off to tell other individuals anything from “Back Off – MY Tree!” to “Hop on and ride me, baby!” But despite how common they are in the rest of the animal kingdom, the function of chemical signals in humans is hotly debated. Years of searching has yet to find human pheromones (no matter what those websites tell you), and while scent seems to play a role in communication in people, there is still relatively little knowledge as to what chemicals and why.

Given that tears are known to serve as sexual signals in mice, it isn’t strange at all that Noam Sobel and his team chose to look at the physiological responses to tears. The Israeli team designed an impressive and unbiased set of experiments to determine if the tears produced by women when sad elicit physiological responses in men separate of the visual or auditory stimuli of a woman crying.

To find out if tears alone acted as chemosignals, the scientists collected tears from women watching tear-jerkers, and as a control, compared their effects to saline rolled down women’s cheeks. Men sniffed the solutions without any knowledge as to what they were during a series of different experiments. In the first, men with a tear-soaked pad under their nose were asked to rate the sexual attractiveness and mood of female faces. While the smell of saline had no effect, men inhaling Eau de Tears consistently rated women’s faces as less attractive, though this had no impact on whether they found the faces happy or sad.

For the second experiment, men sniffed tears before watching a sad movie. While doing so didn’t affect their mood, the smell of tears did elicit a physiological response: men’s faces became more conductive to electricity, which happens when we sweat and is indicative of a psychological reaction. Furthermore, the men self-reported less sexual arousal, which was reflected in their bodies as a 13% drop in saliva testosterone levels.

But to really get to the meat of it, the team threw their male test subjects into an fMRI machine and scanned their brains for activity while sniffing tears. Researchers saw much less activity in the hypothalamus and the fusiform gyrus, both of which are thought to be involved in sexual arousal. All three experiments lead to the same conclusion: the chemicals in women’s emotional tears reduce male sex drive.

The real question, though, is why? Why do men’s testosterone levels tank at the smell of a woman’s tears? The overwhelming answer given by mainstream media (as Rheanna pointed out) is that tears just aren’t sexy. When women cry, so the journalists say, it’s a chemical signal that they don’t want to have sex. Because evolution is all and only about sex… right?

Sorry to burst their bubble, but even when it comes to evolution, it’s not all about sex. Selection also favors survival — because, you know, you can’t have sex when you’re dead*. Thus women’s tears are not necessarily evolutionarily intended to turn guys off. For example, Ed Yong brings up the hypothesis that tears might be used to downplay aggression. Think about it: we cry when we’re sad or physically in pain. In both cases, we’re more vulnerable. Getting others, especially angry men, to be less aggressive towards us in that moment could certainly be a benefit to survival.

Really, the idea that tears are intentionally used as a turn off is a hard sell to an evolutionary biologist. What benefit do women get from not having sex when crying? Does it somehow make them have healthier or more babies? Not for any reason I can think of.

There is, instead, an even more intriguing explanation, one that makes a whole lot more sense. Many who wrote about this paper (including Brian Alexander) mentioned that tears are known to contain a variety of compounds, including prolactin, the hormone which is responsible for making a guy cool his jets after he gets off. But prolactin does much more than ensure a guy stops going at it — it’s a hugely important hormone for nurturing behaviors. In fact, the connection between reduced testosterone and nurturing/bonding behaviors may be the real reason as to why men’s testosterone levels dip upon sniffing tears.

Numerous studies have shown that parental and nurturing behaviors are mediated by prolactin while inhibited by testosterone. For example, research has shown that prolactin levels positively and testosterone levels negatively correlate with a father’s impulse to respond to a baby’s cry. Furthermore, men’s prolactin levels spike and testosterone levels drop in the weeks before their partner gives birth.

It goes beyond babies, too. Decreased testosterone and increased prolactin are strongly implicated in establishing and maintaining relationships. Monogamous men have significantly lower testosterone levels and higher prolactin levels than their single brethren. Furthermore, studies have directly shown that artificially increasing testosterone in a double-blind, placebo-controlled setting makes men less generous to strangers and reduces a person’s empathy for others.

Perhaps prolactin or other chemical signals in tears are directly targeting and activating the nurturing pathway in men’s brains. Being taken care of or protected when in emotional or physical pain would definitely benefit an individual’s survival. Personally, I would like to see this study of tears replicated to determine women’s responses to the scent as well as men’s reactions when using men’s and children’s tears, as well as looking at the levels of prolactin, oxytocin, and other well-established bonding and empathetic hormones. My bet is the response isn’t limited to men, and isn’t limited to emotional secretions from women.

While Brian Alexander and the rest of the sensationalists seem to suggest the signal is “I’m not in the mood,” its likely that the message has nothing to do with having or not having sex. Women aren’t saying “back off” — they’re saying “help me.”

Why do I care so much? It’s not just that they got it wrong. It’s that their interpretation of research isn’t labeled as opinion. It’s that the vast majority of people who have any interest in science news are going to read inaccurate (if not downright insulting) news articles and think studies like this one are either misogynistic or frivolous. It’s that journalists like Brian Alexander undermine good science for the sake of attention grabbing headlines. And as a scientist and a writer, it’s a double insult.

Gelstein, S., Yeshurun, Y., Rozenkrantz, L., Shushan, S., Frumin, I., Roth, Y., & Sobel, N. (2011). Human Tears Contain a Chemosignal Science DOI: 10.1126/science.1198331

* I can hear the comments now, you sickos, so let me clarify: you can’t have baby-producing sex when you’re dead.

Also, thanks to Kira Krend for the thoughtful and hilarious discussion on this topic!

Other References:

Haga S, Hattori T, Sato T, Sato K, Matsuda S, Kobayakawa R, Sakano H, Yoshihara Y, Kikusui T, & Touhara K (2010). The male mouse pheromone ESP1 enhances female sexual receptive behaviour through a specific vomeronasal receptor. Nature, 466 (7302), 118-22 PMID: 20596023
Fleming, A. (2002). Testosterone and Prolactin Are Associated with Emotional Responses to Infant Cries in New Fathers Hormones and Behavior, 42 (4), 399-413 DOI: 10.1006/hbeh.2002.1840
Storey AE, Walsh CJ, Quinton RL, & Wynne-Edwards KE (2000). Hormonal correlates of paternal responsiveness in new and expectant fathers. Evolution and human behavior : official journal of the Human Behavior and Evolution Society, 21 (2), 79-95 PMID: 10785345
Burnham, T. (2003). Men in committed, romantic relationships have lower testosterone Hormones and Behavior, 44 (2), 119-122 DOI: 10.1016/S0018-506X(03)00125-9
Zak, P., Kurzban, R., Ahmadi, S., Swerdloff, R., Park, J., Efremidze, L., Redwine, K., Morgan, K., & Matzner, W. (2009). Testosterone Administration Decreases Generosity in the Ultimatum Game PLoS ONE, 4 (12) DOI: 10.1371/journal.pone.0008330
HERMANS, E., PUTMAN, P., & VANHONK, J. (2006). Testosterone administration reduces empathetic behavior: A facial mimicry study Psychoneuroendocrinology, 31 (7), 859-866 DOI: 10.1016/j.psyneuen.2006.04.002

Grand Opening of Science Sushi!

Welcome to grand opening of Science Sushi!

For all of you who were regulars at Observations of a Nerd – hello again! I hope you like the new name and décor. The menu hasn’t changed – I’m still dishing out juicy portions of biology colorfully spiced with humor and served with the occasional slice of opinion. Click for the new feed url.

To the newcomers, welcome! Let me introduce myself: my name is Christie. I’m a marine biologist by trade. I like cuddly creatures, karaoke, and long walks on the beach, the last of which I get to indulge in often since I am pursuing my PhD at the University of Hawaii. You can get to know me better by checking out my facebook, twitter, or personal website.

This blog is how I share what I love most with everyone I can. My posts have taken the form of essays, news articles and even short stories. They vary in length, breadth and depth, but the common thread which ties them all together is that this is a science blog. That means that no matter what the style, the meat and potatoes of every post you’ll read here is scientific research.

I think science is fascinating – that’s why I have pursued a career in it. I think science is so fascinating that for the longest time, I just couldn’t understand why there are people out there who don’t. Then, about three years ago, I had an epiphany.

I realized that people don’t like science because they don’t know her like I do.

Science isn’t always easy to get along with. She often comes off cold, calculating and condescending – that is, if you can understand a word she says. Her accent can be so bizarre that you’re not even sure you speak the same language she does. Then, by choice or by chance, you spend some time with her. You grab a cup of coffee and end up lost in conversation. You get to know her. And as you do, you stop noticing the peculiar way she phrases things. You find yourself laughing at her jokes and getting swept up in her stories. Suddenly she seems less abrasive, even charming. Before you know it, you’ve fallen completely in love with her.

People would find science as fascinating as I do, I figured, if they really understood the work being done and what is being discovered. The problem is, scientific research is written in a language that takes a dozen or so years of higher education to decipher.

I came to the sudden understanding that science needs professional translators who speak Jargon and English. It was about then that I realized that I just so happen to speak Jargon and English, and was indeed exquisitely qualified to fulfill such a position.

I’ve been blogging ever since.

I hope that you’ll make yourself comfortable and take a look around. I’ll start serving the tasty science writing this blog is all about soon enough, but for now, I’ve included some of my favorite posts from Observations at the bottom of this post to whet your appetite. You can even send me suggestions of topics or concepts you’d like to learn more about – I cook to order!

Also, while you’re waiting, flip through the initial posts from some of the other bloggers with whom I am lucky enough to share a network. I am unbelievably excited to be here at Scientific American and amongst such talent.

Finally, if you like what you see, it would mean the world to me if you help spread the word about Science Sushi and the other blogs on this brand new network. Every little bit helps, whether it’s a tweet, a blog post, a facebook like or a stumble. Mahalo!

– Christie

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