Tag: Evolution

Parasitic flower pirates genes from its host

Rafflesia cantleyi, perhaps better known as the corpse flower for its pungent scent, steals everything from its host. Though each blossom can be in excess of three feet across, the massive buds cannot support themselves, and have no leaves, stalks or true roots. Instead, they rely entirely upon their vine host, Tetrastigma rafflesiae, for survival. Harvard researchers have now discovered that food and water aren’t the only things the corpse flowers steal – over the course of evolutionary history, Rafflesia has also stolen Tetrastigma‘s genes.

The corpse flower and its host have a very intimate relationship. From the start, Rafflesia burrows into the Tetrastigma‘s tissues, growing as thread-like strands in direct contact with the surrounding vine’s cells. They are so dependant on their host that the corpse flowers have even lost the ability to make chlorophyll, a requirement for photosynthesis, and thus defy the very nature of being a plant by being unable to produce food from sunlight. These parasites feed off their host vines, growing and growing until they finally erupt, dramatically if briefly, into large, rubbery flowers that stink like rotting flesh.

Somehow, after generations and generations of intimate contact between parasite and host, Rafflesia has ended up with more than the usual parasitic spoils. As a new study published today in BMC Genomics reveals, the parasite expresses dozens of genes that it has co-opted from its host.

The passage of genes from distant lineages, such as the corpse flower and its vine host, is known as horizontal gene transfer. Though common in bacteria (e.g. the transfer of antibiotic resistance), it is much rarer in plants and animals, and we still don’t fully understand how it occurs.

Scientists were first alerted that something was a little off with Rafflesia several years ago. At that time, they were looking at a much bigger picture – the overall evolution of parasitism in plants – when they noticed something a little odd in their data. For one of the genes, Rafflesia and similarly deeply-embedded parasites didn’t appear to be related to their closest kin, and instead, appeared to be cousins of their hosts. They hypothesized that such a strange evolutionary relationship could only have evolved in one way: if the parasites had stolen that gene.

Now, the Harvard team has sequenced all of the active genes of both the corpse flower and its host to determine how many genes were stolen. Researchers found that 49 of the proteins expressed by Rafflesia – 2% of its transcribed genome – are bootlegged.

“We found that several dozen actively transcribed genes likely originated from the flower’s host,” said Zhenxiang Xi, first author and a graduate student at Harvard University. They also found that most of these genes were incorporated into the parasites own DNA, even replacing similar genes, and another third of Rafflesia‘s own genes have evolved to look more like the vine’s.

The genes that were stolen perform a wide variety of cellular functions, including roles in respiration, metabolism, mitochondrial translation, and protein turnover. Their active expression suggests that they play a key role in the parasite’s survival, but the researchers hope that future research will determine exactly how important these genes are and whether they help the parasite evade detection by the host’s immune system. “These findings might reflect a sort of genomic camouflage, or genomic mimicry for the parasite,” says Charles Davis, co-author and head of the lab at Harvard. A bacterial pathogen of citrus trees, for example, produces a hijacked protein which limits the victim’s ability to detect and remove the intruder.

What’s truly remarkable about this study is that the rate of gene transfer between the vine and its parasitic corpse flower is as high as rates of lateral gene transfer seen in bacteria. Never before have scientists thought that horizontal gene transfer could play such a pivotal role in the evolution of plants and animals, let alone in parasite-host relationships. Given that parasites make up for an astounding 40% of the species on Earth, these findings are bound to transform our understanding of evolutionary processes and how we ended up with the diversity of life we see today.

 

Reference: Xi, Z. & et al, (2012). Horizontal transfer of expressed genes in a parasitic flowering plant, BMC Genomics, 13 DOI: 10.1186/1471-2164-13-227

Rafflesia Image provided by BMC Genomics

The Nose Knows: Telling Age Based On Scent

Our sense of smell is often overlooked. After all, our 20 million smell receptors pale in comparison to the 220 million found in the noses of man’s best friends. We don’t take credit for our ability to distinguish thousands of different smells, even in minute quantities, or how our brains can form strong and lasting memories of scents from a very young age. Yet of all our senses, smell is the first to develop, and before we can feel or see, our noses are hardwired into our brain’s limbic system and amygdala, the parts of the brain where emotions are generated and emotional memories are stored. Since smell detects chemicals in the air, it can warn us of dangers at a distance, even when our eyes and ears are unable to detect them. But more importantly, because it relies on chemicals, smell is one of the most honest ways animals communicate. Human odors, from the smell of tears to underams, have been shown to affect how we think, feel and act, and although we don’t often realize it, our noses play a key role in how we recognize and communicate with one another.

So perhaps it shouldn’t be surprising that scientists have discovered we can distinguish a person’s age by scent alone. In a study published today in PLoS ONE, scientists document how our noses are able to distinguish older people from middle-aged and younger ones not based on the scent mothballs or denture cream, but based on the smell of their body odor.

While we tend to think of B.O. as a reason to wear deodorant, the chemical complexity of Eau de Self is remarkable. Our personal scents can convey a biological and social information, and are thought to play a role in who we like, how we recognize others, and even how we tell men from women. Babies know their mother’s smell shortly after birth, and at a young age we can distinguish between family members and non-family based on their scent. Research has even suggested that we really do have ‘chemistry’ with the people we like, as we can smell immune system differences that might factor into attractiveness, and that we might even be able to smell differences in personalities. Yet there is a lot we don’t understand about how our olfactory system works and exactly what information we obtain through our sense of smell. Given that other animals have been shown to distinguish older animals based on smell, Susanna Mitro and her colleagues from Swarthmore College and the Karolinska Institute in Sweden wondered if smells help us distinguish a person’s age.

To find out, the research team placed pads under the armpits of people in three age groups: young (20–30 years old); middle-age (45–55 years old); and old-age (75–95 years old). Young research participants were then told to discriminate between age categories in side-by-side comparisons and to group the smells according to age as well as rate their perceptual properties like how pleasant or strong the smell. The researchers were startled to find that the participants rated the older aged group’s smell as the most pleasant and least intense. “This was surprising given the popular conception of old age odor as disagreeable,” said co-author Johan Lundström. “However, it is possible that other sources of body odors, such as skin or breath, may have different qualities.” Participants also rated the smell of women to be far more pleasant than the smell of men. But what the researcher’s really wanted to know was whether they could tell the difference between age groups in head-to-head comparisons – and they could.

While the participants were unable to distinguish between young and middle-aged scents, the smell of old age was distinctive. “These data suggest that, akin to other animals, humans are able to discriminate old individuals from younger individuals based on body odor,” write the authors in their conclusion. “The modest effects suggest a limited impact on our everyday interactions but does support previous reports of a unique ‘old person odor’.”

Scientists aren’t entirely sure what makes the smell of older adults different from that of younger people. Studies have found that certain chemicals are present in different levels in older body odor, suggesting that these compounds may serve as biomarkers for old age, but the relevance of these chemicals to age determination has yet to be tested explicitly, and it is unknown whether these chemicals can be detected well by our noses. It’s also unclear whether the ability to distinguish age changes over time. This study focused on young participants as the odor-sniffers, yet it’s possible that the ability to tell age is age-dependent. Older people may lose this ability, or people may be more able to tell ages that are strikingly different from their own. It’s also unclear if the ability to distinguish age has any evolutionary relevance, or if it is simply a byproduct of our more-acute-than-we-think sense of smell.

The researchers also expressed that their study was careful to keep the body odors pure, and thus it is unclear how the scents of hygiene products might affect their results. Does wearing Old Spice actually make a guy appear older, for example? Or does a flowery perfume enhance the youthfulness of a woman? While this study did not explore these questions directly, it has created a foundation for future studies, which may lead to a better understanding not only of our innate ability to determine age by smell but also how our hygiene routines and how product choices affect how we are perceived by others. I can’t wait to see scientists build off these results!

 

Reference: Susanna Mitro, Amy R. Gordon, Mats J. Olsson, & Johan N. Lundstrom (2012). The Smell of Age: Perception and Discrimination of Body Odors of Different Ages PLoS ONE : doi: 10.1371/journal.pone.0038110

Photo of Nose to Nose by XtremeCamera user Lover1969

Sexually deprived Drosophila become bar flies

“He caresses every bottle like it’s the first one he’s had, saying it ain’t love, but it ain’t bad.”

– Ani DiFranco

Rejection stinks. It literally hurts. But worse, it has an immediate and negative impact on our brains, producing withdrawal symptoms as if we’re quitting a serious addiction cold turkey. It’s no wonder, then, that we are tempted to turn to drugs to make ourselves feel better. But we’re not the only species that drowns our sorrows when we’re lonely – as a new study in Science reveals, rejected Drosophila do, too. Scientists have found not only will these sexually frustrated flies choose to consume more alcohol than their happily mated peers, sex and alcohol consumption activate the same neurological pathway in their brains.

Drosophila melanogaster males sure know how to woo a lady. When placed in the same container as a potential mate, a male fly will play her a delicate love song by vibrating one wing, caress her rear end, and gently nuzzle her most private of parts with his proboiscis to convince her that he is one heck of a lover. But even the most romantic fly can’t convince an already mated female Drosophila to give up the goods, so scientists were able to use the girls’ steely resolve to see how rejection affects fly drinking behavior.

“Alcohol is one of the most widely used and abused drugs in the world,” explains lead author Galit Shohat-Ophir. “The fruit fly Drosophila melanogaster is an ideal model organism to study how the social environment modulates behavior.” Previous studies have found that Drosophila melanogaster exhibit complex addiction-like behaviors. So in the controlled setting of Ulrike Heberlein’s lab at the University of California San Francisco, researchers paired male fruit flies with three types of females: 1) unmated females, which were willing and happy to mate; 2) mated females, which actively rejected the men; and 3) decapitated females, which didn’t actively reject the guys but, well, weren’t exactly willing partners either. After the flies were satisfied or frustrated, they were offered regular food and food spiked with ethanol, and the researchers measured which type they preferred to see if there was any connection between sex and drinking.

The flies that were rejected drank significantly more than their satisfied peers, but so did the ones paired with incapacitated girls, suggesting that it wasn’t the social aspect of rejection but sexual deprivation that drives male flies to increase their ethanol consumption (see the video at the end!). This alcoholic behavior was very directly related to the guy fly ever getting laid, for even after days of blue balls, if he was allowed to spend some time with a willing woman, he no longer preferred the spiked food.

What the scientists really wanted to understand, though, was why. What drives a frustrated fly to the flask? So to look at the underlying mechanism of this phenomenon, the scientists examined the flies’ brains. A body of scientific literature has connected one particular neurotransmitter, neuropeptide F (NPF), to ethanol-related behaviors in Drosophila, so it was a logical place to start. A very similar neurotransmitter in our brains, called neuropeptide Y (NPY), is linked to alcoholism.

Increased expression of NPF in mated male brains, as shown through immunochemistry.

The team found that sexual frustration caused an immediate decrease in the expression of NPF, while sex increased expression. Furthermore, when they used genetics to artificially knock down NPF levels in the satisfied flies, they drank as much as their not-so-satisfied friends. Similarly, when the researchers artificially increased NPF levels, flies stayed sober. This is the first time NPF levels have connected sexual activity to drinking. Clearly, NPF levels controlled the flies’ desire to drink, so the team further explored how NPF works in the fly’s brain.

Many animals, including ourselves, possess a neurological reward system which reinforces good behavior. Through this system, we ascribe pleasure or positive feelings to things we do that are necessary for species survival, including sex, eating, and social interaction. Drugs tap into this system, stimulating pleasure which can lead to addiction. Previous studies have shown that flies find intoxication rewarding, so the researchers hypothesized that NPF may play a role in the reward system.

Preference tests showed that artificially increasing NPF levels in the absence of sex or ethanol was rewarding to the flies, confirming the scientists’ hypothesis. This was further supported by the discovery that constantly activating NPF abolished the flies’ tendency to consider ethanol rewarding.

“NPF is a currency of reward” explains Shohat-Ophir. High NPF levels signal good behavior in Drosophila brains, thus reinforcing any activities which led to that state. This is a truly novel discovery, for while NPF and the mammal version, NPY, have been linked to alcohol consumption, no animal model has ever placed NPF/NPY in the reward system.

Understanding the role of NPF in reward-seeking behaviors may lead to better treatments for addicts. “In mammals, including humans, NPY may have a similar role [as NPF],” says Shohat-Ophir. “If so, one could argue that activating the NPY system in the proper brain regions might reverse the detrimental effects of traumatic and stressful experiences, which often lead to drug abuse.” Already, NPY and drugs that affect the function of its receptors are in clinical trials for anxiety, PTSD, mood disorders and obesity. This study suggests that perhaps they should be tested as treatment for alcoholism, too, as well as other reward-based addictions.

Research: Shohat-Ophir, G, KR Kaun & R Azanchi (2012). Sexual Deprivation Increases Ethanol Intake in Drosophila. Science 335: 1351-1355.

Flies turn to drinking after sexual refusal

This sequence of three videos shows a male fly courting and successfully mating with a female fly, another male fly being rejected by a female, and a male choosing to consume an alcohol-infused solution over a non-alcohol solution. Video © Science/AAAS

Images:

Fruit fly from Wikimedia Commons, posted by Thomas Wydra, edited in Photoshop.

Immunochemistry reproduced from Shohat-Ophir, G, KR Kaun & R Azanchi. Science 335: 1351-1355 (2012).

Hydra Watch What They Eat

A picture of a hydra, from the Encyclopedia of Life

Upon first glance, hydra seem like remarkably simple creatures. The basic description of a hydra would be a tube closed at one end with tentacles surrounding a mouth on the other, made of fragile tissue that can be as slim as two cells thick. No gills, no heart, no brain, no eyes – of course, it would be hard to pack all those organs into a creature a few millimeters long, and hydra certainly seem to do well enough without them. These small relatives of jellyfish are found worldwide, and are some of the only members of the phylum Cnidaria to be found in fresh water.

Yet their modest body plan is misleading. Hydra have fascinated scientists for centuries, for they have a phenomenal capacity to regenerate and may even be immortal. In 1744, Swiss naturalist Abraham Trembly was one of the first to be entranced by these simple animals and reflected, “It seemed to me from the start of my observations that knowledge of the remarkable properties of the polyps could bring pleasure to the inquisitive and contribute something to the progress of natural history.”

The hydra’s simple nature is also belied by their tentacles, which inject a potent neurotoxin into unsuspecting prey using extremely sophisticated cells called cnidocytes. For decades, scientists have sought to understand how these specialized attack cells are triggered. Now, evidence published in BMC Biology suggests these primitive creatures may ‘see’ more than we realized, as the firing of these prey-catching stinging cells is regulated by the same chemical pathway used in our eyes.

Ever since the genome for Hydra magnipapillata was published in 2010, it was known that hydra possess the genes for opsins, the photosensitive protein family found in all animals that can see, but no one knew exactly what they do with them. Unlike other animals, hydra don’t have eyes or eye spots, or any kind of centralized visual sensory area, although they have behavioral responses to light. When David Plachetzki teamed up with Caitlin Fong and Todd Oakley’s lab at UC Santa Barbara, they found that these light-sensitive proteins were clustered on the hydra’s tentacles and around the hydra’s mouth, suggesting that they might be involved in feeding behavior.

Fluorescent picture of hydra tentacle bulbs; Musculature is stained green, neurons, including cnidocytes, are stained red and nuclei are stained blue

In hydra, potent stinging cells are grouped with other neurons in what are called “battery complexes” on the hydra’s tentacles, forming one of the most intricate systems of neurons in an organism that lacks a central nervous system. Using fluorescent molecular probes, the researchers were able to show that opsins are expressed in the same locations. They also discovered that other proteins that are part of the response to light, cyclic nucleotide gated (CNG) ion channel and arrestin, are found in these battery complexes, too. In other words, the stinging arsenals are completely equipped to react to changes in light.

Just because they have the parts, however, doesn’t mean they use them. So to see if the stinging cells themselves, the cnidocytes, are regulated by light, the researchers exposed hydra to LED lights of different intensities, then prodded the animals’ tentacles with gelatin-coated fishing wire as if they were being touched by potential prey. After, the team was able to count how many cnidocytes were embedded in the line as a way of measuring whether the stinging cells were triggered.

They found that bright light decreased the firing of stinging cells – which makes sense, really. “Cnidocytes are expensive to make for a hydra; a significant proportion of their cellular mass is comprised by these cell types. Therefore, it is important these austere animals to discharge them in an economical manner,” explains Plachetzki. Hydra and their relatives in the phylum Cnidaria are known to feed in daily patterns, becoming especially active at dawn or dusk, so it’s logical that they would be less inclined to feed in bright light, which might be perceived as day. Of course, there is an even more straightforward explanation as to why cnidocytes fire when the lights go out – shadows. “It could be that hydra use this sensory function to detect the shadows cast by prey on feeding tentacles, just when the moment is right to strike.” The researchers were able to directly connect the opsin signaling cascade to this change in feeding behavior by introducing a blocker of opsin signaling, cis-diltiazem. In the presence of the blocker, light had no affect, confirming that opsin-based signaling is required for this light-mediated change in cnidocyte firing.

Since hydra have been extensively studied for centuries, it is a bit surprising that we are only now learning how light affects their feeding. “It is strange that nobody had discovered this before,” remarked Plachetzki. “Folks have been playing around with hydra and their photobehavior for greater than 200 years, why didn’t they notice this?” But, he says, when you look at some of the older observations of these creatures, “you get the impression that others might have had this hypothesis as well, but there were until now never any data to support it.”

These findings reveal one of the earliest uses of the chemical pathways that were co-opted to create vision. By learning more about these signaling cascades, we can begin to glimpse back at the very beginnings of sight, and slowly learn more about the evolutionary steps that led to our eyes. Aside from the interesting evolutionary implications, this research may also lead to more direct benefits to humans. Cnidarians, including hydra, jellies and corals, are responsible for tens of thousands of stings every year, a handful of which are fatal. The more we know about how these stinging cells are triggered, the better we can prevent these stings, or even develop a way of protecting swimmers against them.

Reference: David C Plachetzki, Caitlin R Fong and Todd H Oakley (in press). Cnidocyte discharge is regulated by light and opsin-mediated phototransduction. BMC Biology

The Sweet Taste of Fear

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.

Now, a team from Singapore has identified that the elusive Schreckstoff as the same compound that we take to improve our joints and treat osteoporosis: chondroitin sulfate.

Structure of Chondroitin Sulfate (c/o Wikipedia)
Structure of Chondroitin Sulfate (c/o Wikipedia)

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.

Brain scans showing chondroitin-stimulated brains in comparison to controlsBecause 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:

Zebrafish fear response to Schreckstoff

Darwin’s Degenerates – Evolution’s Finest | Observations

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.

An ant being attacked by a parasitoid phorid fly. Photo Credit: Bernardo Segura

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?

A malaria-infected blood cell. Image Credit: NIAID

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

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.

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.

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

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:

human-evolution.gif

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.

Originally posted Nov 1st, 2010.

ResearchBlogging.orgReferences:

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 24th, 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. Monarcha castaneiventris megarhynchus (chestnut) and a subspecies on neighboring satellite islands, Monarcha castaneiventris ugiensis(black)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.

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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