Climate Change and Evolution

Posted on May 2, 2014 by Sarah Rivard Meadows

Contributed by Sarah Meadows

Climate change has the potential to shape evolutionary change in species, and has already done so in a few species around the planet. Climate change, or global warming as it is also called, can exact selectional pressure on species because of how it changes the habitat. Changing temperatures is perhaps the most well-known effect of climate change. Climate change can exert selectional pressure because not all species are fit enough to survive when their habitat changes.

One of the challenges with studying climate change and evolution is that it can be hard to distinguish between plastic responses and genetic changes. Plasticity is a species’ ability to adapt to changing conditions without their genetics, or their DNA, being changed. If a species breeding time is earlier than before and there is a correlation with warmer temperatures, for example, it could be because most individuals have the ability to begin breeding earlier (a plastic response), or it could be because individuals that happen to breed earlier have higher survival and reproduction, and they pass this early breeding trait onto their offspring. The latter scenario represents evolution by natural selection. Much of the research done so far on the subject has measured a change in life history traits but has not determined if the cause is a genetic change or phenotypic plasticity.

Species can respond to climate change in a few ways. They can change their life history traits, they can expand or shift their range, or they can go extinct. The latter has already happened to some amphibian populations, such as the golden toad and Monteverde harlequin frog in Costa Rica.

Some species that have been studied extensively on the subject are Drosophila flies, Darwin’s finches, and many other bird species. Some Drosophila have been found to exhibit genetic changes in the northern ranges that are very similar to ones from their southern ranges, suggesting that they either migrated northwards or there was directional selection for those genes. Some other changes that have been observed in other species due to climate change are ranges moving northwards, egg laying and breeding periods happening earlier, and migration happening later.

A few species of Drosophila have recently experienced genetic changes that have been attributed to climate change.

Even though some species have the ability to respond to climate change, such as adapting to the new conditions or moving, not all species can do so. Amphibians, for example, are hit very hard by it, with high rates of extinction compared to other vertebrates. Coral reefs are also hit hard by climate change because higher CO2 levels and bleaching (losing their microbial partners) is a problem. Another problem that is posed by climate change is that if two species have coevolved and are symbiotic with each other, one species could experience evolution due to climate change and the other may not. For example, a pollinating insect could emerge too early before the plant species it usually pollinates has bloomed.

Artic terns are one species of birds whose breeding date has advanced, possibly because of climate change. This is an example of a phenotypic change.

Insects can be affected by asynchrony, for example when a butterfly hatches earlier then its host plant.

Climate change presents a new, challenging influence on habitats, and its long term effects on species diversity and their evolution have yet to be determined, but in the short term it is clear that climate change does have an effect on the evolution of species.

For more information, see:

Balanyá, J., Oller, J. (2006) Global Genetic Change Tracks Global Climate Warming in Drosophila subobscura. Science. 313: 1773-1775.

Gienapp, P., Teplitsky, C., Alho, J. S., Mills, J. A. and Merila, J. (2008), Climate change and evolution: disentangling environmental and genetic responses. Molecular Ecology, 17: 167–178.

Grant, P., Grant, R. (1995), Predicting microevolutionary responses to directional selection on heritable variation . Evolution, 49: 241-251.

Levitan, M., Etges, W., (2005) Climate change and recent genetic flux in populations of Drosophila robusta. BMC Evolutionary Biology, 5:4

MØller, A. P., Flensted-Jensen, E. and Mardal, W. (2006), Rapidly advancing laying date in a seabird and the changing advantage of early reproduction. Journal of Animal Ecology, 75: 657–665.

Parmesan, C. (2006), Ecological and evolutionary responses to recent climate change. Annual Review of Ecology Evolution and Systematics, 37: 637-669.

Pounds, A., Bustamante, M. (2006), Widespread amphibian extinctions from epidemic disease driven by global warming. Nature, 439: 161-167

The Evolution of Bitter Taste

Posted on May 1, 2014 by Robert Christopher Bruner

Contributed by Jonathan Adcock, Hana Ahmed, Robert Bruner, Farhan Momin, Andrew Shibata

How Bitter Taste Works

Specialized bitter taste receptors are concentrated at the back of the tongue. Upon eating a bitter food, these receptors are activated, and and a signal is sent to to the brain that leads to the perception of a bitter taste. Bitter taste receptors are encoded by the TAS2R gene family. This family includes nearly 25 genes and psuedogenes (genes that are no longer functioning) that are concentrated in bundles on chromosomes 3, 5, and 7. Extensive studies have been performed in order to determine which molecules in bitter foods can activate these receptors. Scientists have found that many of the compounds that activate the bitter taste receptors are chemicals produced by plants. Many of these compounds were also found to be toxic and if consumed could lead to illness or death.

How Bitter Taste Evolved

Our ancestors and other animals have not always been able to taste bitter foods. The bitterness sensation is thought to have evolved 200 million years ago. The prevalent hypothesis is that bitter taste evolved by random gene mutation events which caused the formation of the TAS2R gene family and the bitter taste receptors on the tongue that could bind to toxic chemicals. Animals possessing these mutations were able to taste toxins in their food. These toxins would have tasted bad to the animal, and thus, the animal would learn to avoid the toxic food in the future. Animals with the mutations that produce the TAS2R gene family would be be better adapted to their environment because they can avoid toxic and poisonous foods that could cause sickness or death in the animal. Animals not possessing these mutations would still be susceptible to ingesting naturally occurring poisonous chemicals. Because these animals have improved survivability in comparison to other animals without the TAS2R genes, animals that could taste bitter foods would be better able to reproduce and pass the functional TAS2R genes to their offspring, who in turn would have increased survivability, be better able to reproduce and pas the TAS2R genes to their offspring. Organisms possessing the TAS2R genes have a higher fitness than organisms that do not posses this gene family. Thus, the TAS2R gene family would have been selected for via natural selection and became the ability to taste bitter foods would have become dominant in the population.

This is especially true in the case of the thyroid-inhibiting toxin, PTC. PTC is known to decrease thyroid hormone, which regulates metabolic function. PTC can also lead to liver damage and a host of other medical problems that would eventually lead to death. Being able to taste the PTC toxin would have allowed our ancestors to to avoid toxic foods that if ingested would ultimately lead to their death. Because of this, the ability to taste the PTC toxin would be passed on to the next generation and contribute to the increased fitness of the following generation. In this way, the bitter taste genes would become selected for and would become prevalent in the population.

How the Evolution of Bitter Taste Affects Me Today

Although variation in taste facilitated the evolution of primates and other animals, in modern human society it can be detrimental. With the advent of agriculture, there is less need for tasting of bitter food. Highly nutritious vegetables are known to activate the bitter taste receptors. Instead of doing their intended evolutionary job of protecting from toxic materials, the bitter taste receptors are preventing some people from getting an adequate daily amount of nutritious vegetables due to their aversive taste.

Additionally, some individuals have extremely high sensitivity to bitter tastes resulting from higher rates of expression of the TAS2R gene. These individuals are known as “supertasters”. Supertasters can be found in the highest frequency in parts of Asia, Africa, and South America. This may be because these areas originally possessed a higher concentration of toxic plants and animals in comparison to other areas. In order to compensate for the increase in potential toxins, the individuals living in this area might have benefited more from bitter taste receptors. Today, many supertasters dislike a wide variety of vegetables such as cabbage and soy, and favor sweet items over bitter vegetables. This not only leads to increased chance of obesity and diabetes, but because of the avoidance of vegetables there is increased risk for GI diseases such as colon cancer. Not all side effects are bad though. Supertasters have a higher dislike for alcohol, carbonated beverages, and smoking. Avoidance of these items is actually quite beneficial in boosting heath.

Next time you don’t feel like eating your vegetables, you can blame it on evolution!

The Plight of the Gummy Bears

Posted on April 30, 2014 by Joshua Lee

by Adrian Kinkead, Taara Rangan, Tiffany Liao, and Joshua Lee

The Basics of Gummy Bear Selection

Natural selection is a force that acts upon life on Earth, and works in tandem with evolution to produce fitter populations in a given environment. We often think of evolution as a linear phenomenon, but it is more accurate to think of it as a branching tree of trial and error. The idea that a structured process of adaptation is appealing to us; it imposes an attractive order on the natural world. But the challenges of survival are also arbitrary, meaning the strongest and the fastest don’t always have the advantage in the face of a novel threat.

Imagine a population of gummy bears, living together on their red planet.

Against this red background, the red bears are not easily seen to the eyes of the predators, but the other bears are not so lucky. Even though the red bears aren’t stronger, smarter, or faster than the others, selective pressures are random, meaning those attributes aren’t always relevant. It would follow that the majority of bears who were able to survive predation would be red.

However, life is always changing. Imagine that this red planet suddenly turned green as a forest sprang up overnight. Now, the red bears are very visible to predators. Shown no mercy, the red bear population would be easily reduced, while the green bears (who had clashed with the surface of their red planet) could blend instead.

It is easy to see natural selection as this locomotor that operates outside of the human world, but we are just as malleable to natural selection as any other species on Earth. For example, researchers at the Research Center for High Altitude Medicine found that Tibetans carry a mutation that allows them to thrive in elevations that would be burdensome on humans of other populations. When foreigners visit the summit of Mt. Everest, they must pace their elevation to allow for their blood cell count to increase in order to make up for the lower oxygen availability at that elevation. However, the observed blood cell count in Sherpas and the Tibetans remained at a baseline level. Furthermore, the study revealed that no difference in tissue oxygen concentration was observed either, despite the Sherpas and Tibetans being significantly stronger at those elevations. Researchers observed significantly higher levels of EPAS1 expression, and while the mechanism for its function is not known, they were able to confirm that this mutation accounts for the difference in physiological traits in the Tibetans and Sherpas (Simonson, et al.).

Gummy Bear Mimicry and Selection

But life isn’t just about colors. Imagine that a few of the bears developed a toxin in their bodies that cause painful stomachaches in their predators, and also produce a very bright red pigment. Predators would think twice before snatching up an easy catch of red bears and opt for other colors instead. Furthermore, the nonpoisonous red bears, despite being a duller red than their poisonous counterparts, also enjoy safety; their color is associated with discomfort and pain, causing the predators to ignore red bears altogether.

But the nonpoisonous gummy bears only receive such an advantage because the poisonous ones are so few and far between. If the poisonous ones become more numerous, predators would have an easy time of comparing the nonpoisonous red gummy bears to their brighter, redder counterparts. And so, the protection afforded to the nonpoisonous bears disappears. There may be a moment of hesitation, but predators will no doubt go back to preying on the hapless dull red gummy bears, leaving the poisonous ones alone.

This method of mimicry, known as Batesian mimicry, is not a perfect disguise however, as some predators can distinguish between dangerous and harmless prey. In a study conducted by researchers, Kraermer and Adams, they found that two salamander species, a model and mimic, would elude snake and mammal predators by color association alone. However, bird predators were able to distinguish between the palatable and toxic salamanders by their distinguishing patterns.

The organisms seen today are reflections of eons of environmental changes and selective pressures. Our DNA bears the markings and scars of cataclysmic events and relationships with other kinds of life around us. Natural selection explains the mechanism that allows organisms to evolve as a species. It acts on individuals to affect the whole, but it must be made clear that it does not evolve an individual specifically. It allows for the emergence of different attributes that can be passed on to future generations and define entire new species.

http://youtu.be/XS-pUWLtVe4

More resources on selection and mimicry can be found in:

Johnstone, Rufus A. “The Evolution of Inaccurate Mimics.” Nature 418.6897 (2002): 524-26.

Kraemer, Andrew C., and Dean C. Adams. “Predator Perception Of Batesian Mimicry And Conspicuousness In A Salamander.” Evolution 68.4 (2014): 1197-206.

Losos, Jonathan B., Thomas W. Schoener, and David A. Spiller. “Predator-induced Behaviour Shifts and Natural Selection in Field-experimental Lizard Populations.” Nature 432.7016 (2004): 505-08.

Morgans, Courtney L., and Terry J. Ord. “Natural Selection in Novel Environments: Predation Selects for Background Matching in the Body Colour of a Land Fish.” Animal Behaviour 86.6 (2013): 1241-249.

Skelhorn, J., and G. D. Ruxton. “Predators Are Less Likely to Misclassify Masquerading Prey When Their Models Are Present.” Biology Letters 6.5 (2010): 597-99. Print.

Simonson, T. S., Y. Yang, C. D. Huff, H. Yun, G. Qin, D. J. Witherspoon, Z. Bai, F. R. Lorenzo, J. Xing, L. B. Jorde, J. T. Prchal, and R. Ge. “Genetic Evidence for High-Altitude Adaptation in Tibet.” Science 329.5987 (2010): 72-75. Print.

Speed, Michael P., and Graeme D. Ruxton. “Imperfect Batesian Mimicry and the Conspicuousness Costs of Mimetic Resemblance.” The American Naturalist 176.1 (2010): E1-E14.

Are Humans Still Evolving?

Posted on April 29, 2014 by Kevin O'Neal Childress

Contributed By Kevin Childress, Ricardo Acevedo, and Crystal Seales

Can we be at the mercy of evolution?

A common misconception about evolution is that humans are no longer evolving. It’s very easy to think that because we seem to be the masters of the world around us, there is no need for the human species to be changing anymore. However, if we just look at some examples, we can see that humans are indeed not immune to the power of natural selection. For example, only certain human populations, mainly from pastoral/cow farming heritage, have the ability to digest milk at older ages. If you contrast those humans with humans from East Asia, you see that a large majority from East Asia cannot digest milk due to the lack of dairy in their ancestor’s diets. (For more information, see a recent post on lactase).

But let’s take a look at a more “drastic” example, the pygmy humans. They represent a population of humans around the world that have an unusually small body size that is well proportioned. They are found in certain African, Southeast Asian and South American populations, so they aren’t just an isolated group of people. The groups found in Central Africa are known to be the shortest humans on Earth! These pygmy populations tend to grow at a slower rate than other humans, and they normally stop growing at just 13 years old!

So why are they short? Well, genetic testing has shown that these groups evolved separately from one another. Currently, many hypotheses are being investigated. The most recent one is that this is an adaptation that allows the pygmies to stop growing at an earlier age, and thus reproduce at a younger age. This is plausible because less resources are put into their growth, allowing for more energy to be available to reproduce at an earlier age. Understandably, however, the hypothesis is highly debated. Others believe that earlier reproduction times and a smaller body size evolved to compensate for a lack of food and resources in their environment. A shorter stature could also help the pygmies navigate their surroundings and regulate their body temperatures more efficiently.

These hypotheses are an attempt by researchers to explain why the pygmy populations differ physically from the rest of the human species. Even though evidence doesn’t support a specific hypothesis at this time, the current data illustrates that evolution is a force that will continue to influence our species.

Check out our video on the topic!

https://www.youtube.com/watch?v=oYWNP0o5f00

For more info, see :

Migliano, A. B., Romero, I. G., Metspalu, M., Leavesley, M., Pagani, L., Antao, T., & T Kivisild. 2013. Evolution of the Pygmy Phenotype: Evidence of Positive Selection from Genome-wide Scans in African, Asian, and Melanesian Pygmies. Human Biology 85, 251–284.

Becker, N. S.A., Verdu, P., Froment, A., Le Bomin, S., Pagezy, H., Bahuchet, S. & E Heyer. 2011. Indirect evidence for the genetic determination of short stature in African Pygmies. Am. J. Phys. Anthropol. 145: 390–401.

Simmons, R.E., & L. Scheepers. 1996. Winning by a Neck: Sexual selection in the evolution of giraffe. The American Naturalist. 148: 771-786.

Migliano, A.B., L. Vinicius, & M.M. Lahr. 2007. Life history trade-offs explain the evolution of human pygmies. Proceedings of the National Academy of Sciences of the United States of America 104.51: 20216–20219.

Meazza, C., Pagani, S., & M. Bozzola. 2011. The pigmy short stature enigma. Pediatric Endocrinology Reviews. 8: 394-399.

Human Impact on Altered Behavior and Evolution of Species

Posted on April 29, 2014 by Brad William Richardson

Contributed by Brad Richardson

A common misconception about evolution is that it is only a theory; however, it is a fact. A fact is a truth known by actual experience or observation. Darwin’s Theory of Evolution by Natural Selection on the other hand is a theory much like the theory of relativity or gravity; it is a broad explanation of a particular phenomena that is proposed based on multiple observations and can be used to make predictions.

Many believe the theory is not testable or observable and that if it is true, it only happens over a very long period of time. However, human intervention via our technological advances such as city building and industrialization has led to an altered environment that is changing at an extreme rate. Although this can have either negative or positive consequences for varying species, one positive consequence for the human species is that it is allowing us to get a much better understanding of the scope and specificity of how evolutionary mechanism works.

Because of this accelerated rate of technological advance by humans, others species are having to adapt and evolve at an equally fast rate. This allows us to get a unique glimpse of evolution happening before our eyes. One of the biggest culprits is of course the effect climate change is having on all species, including our own. Various animals are breeding earlier in the spring, becoming smaller to keep their body temperatures in balance, and even completely moving their ranges away from the equator to avoid the heat!

Many changes are also occurring at the microscopic level due to technological advances in medicine. Antibiotic resistant bacteria have evolved to increase their chances of survival. The bacteria evolve and reproduce at such a fast scale that “superbugs” even exist which evolve resistance to the antibiotics that are usually given as an alternative to regular antibiotics.

Changes are happening all around us, which makes the Theory of Evolution such an interesting topic to study because every day species are changing and adapting and providing “natural” observable data that further bolsters the legitimacy of the theory.

Take a look below at some examples of observable evolution!

https://www.youtube.com/watch?v=fioFFtvEXBw

For more information check out:

Candolin U, Nieminen A, Nyman J. 2014. Indirect effects of human-induced environmental change on offspring production mediated by behavioral responses. Oecologia. 174: 87-97.

Janssens L, Khuong DV, Debecker S, Bervoets L, Stoks R. 2014. Local adaptation and the potential effects of a contaminant on predator avoidance and antipredator responses under global warming: a space-for-time substitution approach. Evolutionary Applications. 7: 421-430.

Sol D, Lapiedra O, Ganzalez-Lagos C. 2013. Behavioural adjustments for a life in the city. Animal Behaviour. 85: 1101-1112.

Nemeth Z, Bonier F, MacDougall-Shackleton SA. 2013. Coping with uncertainty: integrating physiology, behavior, and evolutionary ecology in a changing world. Integrative and Comparative Biology. 53: 960-964.

Martin J, Lopez P. 2013. Effects of global warming on sensory ecology of rock lizards increased temperatures alter the efficacy of sexual chemical signals. Functional Ecology. 27: 1332-1340.

Miranda AC, Schielzeth H, Sonntag T, Partecke J. 2013. Urbanization and its effects on personality traits: a result of microevolution or phenotypic plasticity?. Global Change Biology. 19: 2634-2644.

The Sad History of HIV and its Persistence against Drug Therapy

Posted on April 28, 2014 by Oliver Ting

Contributed by Oliver Ting, Jackson Fritz and Milan Patel

According to a report from the World Health Organization, human immunodeficiency virus (HIV) infected about 2.7 million new people in 2010 alone. Broken down, HIV destroys the immune system in humans, allowing opportunistic diseases to come in and kill the patient. HIV spreads through bodily fluid from person to person. Once inside a patient, HIV targets certain cells within the immune system called T-cells. HIV forces these cells to create new copies of the virus and destroys the T-cells in the process. As the virus grows exponentially, the immune system loses its ability to fight other diseases, leading to acquired immune deficiency virus (AIDS).

HIV cannot be cured. The main problem in creating a drug that treats HIV is that the virus is constantly changing. HIV is a retrovirus, meaning it uses RNA and then converts that into DNA when it infects cells. Retroviruses use an enzyme called reverse transcriptase to do this. However, unlike DNA enzymes, this enzyme cannot proofread itself, allowing more mutations (changes in the genetic code) to occur. This causes the virus to produce a base mismatch roughly every 10, 000–30, 000 bases during the replication. This differs significantly from regular viruses that typically have a range of one base mismatch per one million to one billion base pairs. When these base mutations occur in specific regions of the HIV DNA, new types or subtypes of the virus can be created. HIV builds up drug resistance because a drug that was effective for a previous variation of HIV may not be effective against a new variant of the virus. In addition, the virus builds cross-resistance, and becomes resistant to multiple types of HIV drugs within the same class. This further limits the number of drugs that can be used to treat the virus.

HIV is a prime example of evolution in action. HIV’s high rate of DNA mutation creates many variants. When HIV is selected against through antiviral drugs, certain variants survive that are resistant to the drug. These drug-resistant strains of HIV survive to reproduce and can be transmitted to other individuals. This constantly changing HIV population produces a substantial obstacle in trying to treat and eradicate the virus. Continued research is required to combat this evolving virus and improve the quality of life of those affected by HIV and AIDS.

Inspired by Radiolab “Patient Zero”, a fascinating tale about how HIV began, where it came from, and who “Patient 0” may have been. The podcast further reinforces how the virus has been able to combat so many challenges to its existence as well as it has.

Superbugs: The Evolution of Gonorrhea

Posted on April 28, 2014 by Kari Camille Tyler

Contributed by Nyasia Jones, Chris Richardson and Kari Tyler

https://www.youtube.com/watch?v=AesE046gtQs

A common misconception regarding evolution it that it is slow, and because it is slow, humans are not influencing it. This is completely false. Humans have and are continuing to make major changes that are not only influencing the course of our own evolution, but are also influencing the evolution of other species we interact with. Especially in medicine, human advancement is occurring at an amazing pace and thus allowing us to witness evolution in response to our actions.

Over the past century, the use of antibiotics to treat bacterial pathogens has become a widespread practice. Starting around 1930, medical practitioners began discovering several drugs that successfully rid patients of a particular bacterial pathogen Neisseria gonorrhoeae. The first successful therapy was administration of a class of chemicals called sulfonamides. For years, treatment with sulfonamides proved successful in patient after patient until about the mid-1940s when reports of N. gonorrhoeae resistance to sulfonamides increased. Fortunately, at this time, the “miracle drug” penicillin was found to be highly effective at bacterial treatment and become the number one treatment option. After ten to fifteen years though, low doses of penicillin were no longer as effective, and by the 1980s strains with high-level penicillin resistance had emerged.

So what happened with both penicillin and the sulfonamides? Nothing.

But something did happen to the N. gonorrhoeae. They evolved.

Sequential chromosomal mutations allowed some bacteria to incur resistance to penicillin. With penicillin treatment, the bacteria with resistance survived while those without it did not. The resistant individuals reproduced thereby creating a new generation of bacteria in which all individuals were penicillin resistant. This, my friends, is evolution.

Unlike the billions and billions of years it took to create modern-day humans, this evolution took less than a century to change these N. gonorrhoeae bacteria into “superbugs” which are becoming increasingly harder to treat. And it doesn’t stop there. N. gonorrhoeae has also become resistant to more recent treatment options, such as tetracycline and fluoroquinolones. Now, with less and less success to current methods of treatment, namely cefixime and ceftriaxone, scientists are worried history will repeat itself and strains of N. gonnorhoeae with complete cefixime and ceftriaxone resistance will emerge. With dwindling options for treatment, N. gonorrhoeae resistance and that of other superbugs remains a major problem in the fields of medicine and epidemiology.

So are humans influencing evolution? N. gonorrhoeae tell us, loud and clear: yes!

For more information:

Anderson, M. T., & Seifert, H. S. (2011). Neisseria gonorrhoeae and humans perform an evolutionary LINE dance. Mobile Genetic Elements, 1(1), 85-87.

Mavroidi, A., Tzelepi, E., Siatravani, E., Godoy, D., Miriagou, V., & Spratt, B. G. (2011). Analysis of emergence of Quinolone-resistant gonococci in Greece by combined use of Neisseria gonorrhoeae multiantigen sequence typing and multilocus sequence typing. Journal of Clinical Microbiology, 49(4), 1196-1201.

Unemo, M., & Shafer, W. M. (2011). Antibiotic resistance in Neisseria gonorrhoeae: Origin, evolution, and lessons learned for the future. Annals of the New York Academy of Sciences, 1230(1), E19-E28.

Forget Harry Potter… Check Out the Bobtail Squid’s Invisibility Cloak!

Aside

Contributed by Kelly Costopoulos, Taylor Werkema, and Nina Zook.

One of the most spectacular biological phenomena is an organism’s ability to luminesce. The light can be produced through chemical reactions in specific cells and even, in more rare cases, through a symbiotic relationship of an organism and unique bacteria. An extraordinary example of this is the cooperative relationship between the Bobtail squid and the bacteria Vibrio fisheri.

The Bobtail squid lives in the coastal waters off the Pacific Ocean and some parts of the Indian Ocean. During the day the squid buries itself in the sand and at night it comes out to hunt. The squid mimics the moonlight by using luminescent V. fischeri and eliminates its shadow on the ocean floor below to avoid predators. It’s nature’s own invisibility cloak!

This incredible act starts every morning when free living bacteria in the water are taken up by special light organs in the squid’s mantle. There, they are nourished by special cells that promote the growth of only V. fischeri, all other competitors are actively selected against. Once the bacteria population reaches a certain density, the bacteria produce light. The squid has the ability to control the intensity of light through specialized filters to match the moon’s light exactly. When the sun comes up in the morning, the squid expels the bacteria in a process known as venting, and the cycle starts over.

The video above gives a graphical representation of how the squid uses its invisibility cloak. As the moon comes out, the squid becomes luminescent and its shadow on the ocean floor disappears. This hides the squid from predators below.

The bobtail squid is only one of many squid species in the sepiolid family with V. fischeri symbionts. How did such an intricate symbiosis evolve in these squid species? Because both organisms can be easily cultured and raised in the laboratory setting, researchers can do evolutionary studies to shed light on how and why the sepiolid squid-V. fischeri system has evolved. Researchers have determined the relatedness between similar squid species and the relatedness of their symbiotic bacteria. Interestingly, the bacterial tree lines up with the squid tree, indicating that the squid and bacteria of each symbiotic pair have coevolved. This means that as squid species diverged from one another, so did their native bacteria such that the bacteria became more host-specific.

Evolutionary studies have also helped us understand how bacteria compete to establish symbiosis with the their squid hosts. Experimental competition, or raising a squid in the presence of two different bacteria, has shown that a squid’s native bacterial symbiont will outcompete nonnative strains. Further, the more closely related the nonnative strain is to the native bacteria, the more competitive it will be in inhabiting the squid’s light organ. Thus, the evolutionary history of sepiolid squid species and their unique symbionts is one of fidelity and preference for the native strain with whom the squid has evolved intimately over time.

For more on the squid-vibrio system, check out:

McFall-Ngai, M. 2008. Hawaiian bobtail squid. Current Biology : CB, 18(22), R1043–4.

Nishiguchi, M.K., Ruby, E.G., & McFall-Ngai, M.J. 1998. Competitive dominance among strains of luminous bacteria provides an unusual form of evidence for parallel evolution in sepiolid squid-vibrio symbioses. Applied and Environmental Microbiology 64(9): 3209-3213.

O’Brien, Miles, and Marsha Walton. “Glowing Squid.” National Science Foundation. The National Science Foundation, 22 Nov. 2010. Web. 28 Apr. 2014.

Learning in Lizards

Posted on April 28, 2014 by edlake

Contributed by Elsa Lake

You may have heard about the relative intelligence of some animals, such as dolphins or chimpanzees. However, other animals are not just mechanistic beings. They too have individual variation, including variation in intelligence. An Australian lizard named the Eastern Water Skink (Eulamprus quoyii) was tested for variation in spatial learning performance. An enclosure was set up with a “safe” refuge and an “unsafe” refuge. The lizards were scared around the enclosure until they entered the “safe” refuge. If they entered the “unsafe” refuge, then the refuge was lifted and scaring the lizard resumed.The spatial learning task given to the lizards was learned by twice as many males as females.

Nature presents different challenges to males and females; males are more successful at passing on their genes if they mate with as many different females as possible, and females are more successful if they select males with the highest quality genes to mate with. It is suggested that males have more spatial challenges, such as location of rival males, to deal with, so males would be better at spatial tasks overall.

A “Boldness” Experiment. One refuge was designated the “hot” refuge, and the other the “cold” refuge. Lizards prefer the “hot” refuge because they are cold blooded, and need the external heat to warm up their bodies and get energy, similar to a person who wants to bask in the sun at the beach! However, in the experiment, the lizards were scared off the basking refuge into the “cold” refuge. Researchers measured the time it took for the lizards to return to their basking sites. “Bold” lizards were determined to be those that quickly returned to the basking site, and “shy” lizards took a long time to do so.

The learning task was also more likely to be learned in lizards who were shown to be either very bold or shy, but not likely in lizards with behavior somewhere in between the two extremes. It is suggested that the males in this species of lizard may have evolved so that these two different personalities serve different roles. Territorial lizards are known to actively defend against other males, while “floater” lizards travel from territory to territory in search of mates. These two strategies may be employed by “bold” and “shy” lizards, respectively, while a lizard with a personality in the middle cannot utilize either strategy effectively.

It’s amazing to see how evolution hasn’t caused all Eastern Water Skinks to be the same. There is individual variation in them, just like there is variation in our own personalities. This variation in personality causes us to have different interests, work different jobs, and in general live our lives differently, just as it has caused the male skinks to use different strategies for finding mates. Animals aren’t as different from us as one might think!

See the below papers for more information:

Carazo, P., Noble, D. W. A., Chandrasoma, D., & Whiting, M. J. 2014. Sex and boldness explain individual differences in spatial learning in a lizard. Proceedings of the Royal Society B: Biological Sciences, 281(1782).

Chittka, L., Skorupski, P., & Raine, N. E. 2009. Speed–accuracy tradeoffs in animal decision making. Trends in Ecology & Evolution, 24(7), 400-407.

Noble, D. W. A., Carazo, P., & Whiting, M. J. 2012. Learning outdoors: male lizards show flexible spatial learning under semi-natural conditions. Biology Letters, 8(6), 946-948.

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Venom Variation

Posted on April 28, 2014 by Cherishma Patel

Contributed by Annelise Bonvillian, Cherisma Patel and Liz Pinkerton

I introduce to you two rattlesnakes. I think they’re generally friendly but they could also be planning to maim me. You just never know with venomous snakes.

Judging by their appearance, you’d think both rattlesnakes were of the same species. You’d be right, being the clever person you are. They are in fact part of the same subspecies of Southern Pacific Rattlesnake (Crotalus oreganus helleri).

These C. o. helleri rattlesnakes are venomous. Before we dive into their story, let’s explain venom.

Venom Across The Tree of Life

Many animals have evolved venom for protection or to help them capture prey. We, unfortunately have not.

There are also a wide range of structures for delivering venom, such as the cute little fangs in these rattlesnakes.

The interesting thing is, similar types of venom have evolved in completely unrelated species. This is not because all venomous species evolved from one super venomous ancestor or because the venomous critters of the world get together to talk strategy.

Evolution of venom is a solid example of convergent evolution in which organisms that are not very closely related independently evolve similar traits due to similar environmental pressures. The proteins in the toxin end up acting on the same physiological molecule by chance. Most venoms involve disrupting major physiological pathways that are accessible by the bloodstream, especially the hemostatic and neurological systems. Damaging these systems would efficiently cripple any prey or potential predator.

Back to the Rattlesnakes

Getting back to our original C. o. helleri rattlesnakes, you’d think it might be true that they’d have the same type of venom because they’re of the same subspecies, right?

In fact, these two rattlesnakes are very closely related, but the populations that live in the mountains have a distinctly different venom than those that live in the desert.

Distribution of Crotalus oreganus

A research team from the University of Queensland studied the variation between rattlesnakes in the mountainous area of Idyllwild, California and those in the desert of Phelan, California. The extent of venom variation is surprising for two populations because the two areas are relatively close together geographically.

The venom of the desert-dwelling rattlesnake contains proteins that break down blood vessels and prevent clotting.

This venom is slow acting. It is described as haemotoxic and would lead to uncontrollable bleeding. Neat!

Its close relative in the mountains is equally as morbid. The mountain populations have proteins in their venom that stop nerves from sending signals to the muscles.

This venom is fast acting. It is described as neurotoxic and results in paralysis. Sweet!

The venoms are completely different even though these two populations are from the same subspecies.

In fact, venom can vary between species, subspecies, individuals, sexes, and ages. Another research team from the Biomedical Institute of Valencia that loves poisonous reptiles just as much as the the previous one studied venom variability in Mojave rattlesnakes in Arizona. They found that you were 10 times more likely to die from a bite in one county than another. Here, the severity, not the type, of venom was what varied.

So, getting back to our C. o. helleri rattlesnakes (don’t worry, we love you best), here’s another question: which would be better to have in the snake’s arsenal? The fast acting neurotoxin venom or the slow acting haemotoxin?

Evolution, the lovely process that developed these fine creatures is NOT about having the best of a trait. The fitness of a certain trait is relative. What is good for one population might not necessarily be the best for another. Based on where they live, different venom types might be more beneficial in capturing prey or warding off predators.

So why would it be more beneficial for the mountain rattlesnake to have a faster acting venom?

Researchers suspect that environmental differences between these two populations of rattlesnake are likely to have promoted the huge variation in venom between the two.

If the mountain rattlesnake’s venom was slow acting the, prey could hide before the venom had properly incapacitated it.

And venom isn’t cheap. Creating venom costs a lot of energy and wasting it time and time again would be a shame. Natural selection would thus lead to a venom composition that would reduce metabolic cost. Natural selection is the process by which organisms that have higher fitness and are more adapted to their environment tend to produce more offspring and survive.

Now, in the desert, rattlesnakes don’t have to worry as much about their prey hiding before they can get to them. They might not have evolved the quicker neurotoxic venom because there was no selective pressure to have their venom be fast acting.

As with most things in this incomprehensible universe, we are not sure if the desert dwelling Southern Pacific rattlesnake maintains its haemotoxic venom due to lack of selection pressure. Or perhaps somehow the snakes have co-evolved with their prey and the haemotoxic venom is just the most efficient one for the prey type.

All in all, it’s important to realize that evolution isn’t a race where the end goal is to have the best of something. Traits change randomly due to mutations, and factors such as the environment or prey type select for variations that are most beneficial for survival.

In related news, using the vast powers of human intelligence to learn from the natural world, snake venom is being adapted to heal instead of hurt. Venom works in the same way as many medicines, and the enzymes in venom are being modified to affect disease processes.

One specific example includes the using ACE inhibitors in Brazilian pit viper venom to prevent hypertension.

However, with the decline of snake diversity due to environmental degradation, the diversity of venom and its medical potential is decreasing.The fact that venom from various snakes can be used to target certain diseases is a very important implication for evolutionary medicine. Population divergence in snakes increases the potential for variation in venom type, which can ultimately increase the antidotes possible for fighting certain diseases.

So why research things like rattlesnake venom? Not only is the subject wildly fascinating, but unraveling the complexities of snake venom can help humans better counter its life-threatening effects and can also promote the development of new medicines. In conclusion, though we may be terrified of you, dear rattlesnakes and other venomous denizens of this world, we’d also like to say thanks. May you continue to amaze us.

Check out these sites for more information:

Caswell, Nocholas R., Wolfgang Wuster, Freek J. Vink, Robert A. Harrison, and Bryan G. Fry. 2012. Complex cocktails: the evolutionary novelty of venoms Trends in Ecology and Evolution.

Holland, Jennifer S. 2013. Venom: The Bite That Heals. National Geographic: The New Age of Exploration. http://ngm.nationalgeographic.com/2013/02/125-venom/holland-text

Kartik Sunagara, Eivind A.B. Undheimc, Holger Scheibd, Eric C.K. Grene, Chip Cochrane, Carl E. Persone, Ivan Koludarovc, Wayne Kellne, William K. Hayese, Glenn F. Kingd, Agosthino Antunesa, Bryan Grieg Fry. Intraspecific venom variation in the medically significant Southern Pacific Rattlesnake (Crotalus oreganus helleri): Biodiscovery, clinical and evolutionary implications. 2014. Journal of Proteomics. http://www.sciencedirect.com/science/article/pii/S1874391914000256

Massey DJ, Calvete JJ, Sánchez EE, Sanz L, Richards K, Curtis R, Boesen K. 2012. Venom variability and envenoming severity outcomes of the Crotalus scutulatus scutulatus (Mojave rattlesnake) from Southern Arizona. Journal of Proteomics. http://www.ncbi.nlm.nih.gov/pubmed/22446891

Yong, Ed. 2014. Rattlesnakes Two Hours Apart Pack Totally Different Venoms. National Geographic: Phenomena. Online. http://phenomena.nationalgeographic.com/2014/01/27/rattlesnakes-two-hours-apart-pack-totally-different-venoms/

Zimmer, Carl. 2013. On the Origin of Venom. National Geographic: Phenomena. Online. http://phenomena.nationalgeographic.com/2013/01/09/on-the-origin-of-venom/

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evolution and evolutionary biologists in the natural world

Category Archives: adaptation