The Mystery of Giraffe Necks

Contributed by Grace Lee

Why do giraffes have long necks? The theory is quite more complicated than expected. Although it’s something that we rarely question, evolutionary scientists have been debating the answer to this question for years. Conveniently, this matter addresses a common theme and misunderstanding of evolutionary biology that we can learn from.

To begin, there are two leading hypotheses as to why giraffes have such long cervical vertebrae. The first, known as the ‘competing browsers’ hypothesis, states that their long necks evolved over time to gain the advantage of being able to reach the leaves of tall trees for feeding. The second, known as the ‘necks for sex’ idea, states that this trait evolved as a weapon that allows males to battle each other to gain dominance for mating with females.

A common misconception is that natural selection produces animals that are perfectly suited for their environment. Unfortunately, evolution does not work to create the “perfection version” of an organism. For example, while it seems that it would be advantageous to have the longest neck in the population, studies show that long necks require increased nutrition for maintenance of health and extreme blood pressures to pump blood from the heart to the brain. Furthermore longer necks may attract predators more easily and may slow down escaping. Evolution is filled with many trade-offs in which a trait is beneficial in one context but harmful in another. There could potentially be a giraffe that not only is suitable for battling rivals and feeding off tall trees but also at the same time easily hidden from predators, but evolution may not necessarily be working towards an “upgrade.”

So what is the correct answer? Perhaps, an unsatisfying “both.” The ‘competing browsers’ idea doesn’t work alone because in the driest seasons, when it would seem the most beneficial to have the longest neck to reach for leaves no other animals could, giraffes tend to feed from shrubs. Even ordinarily, giraffes often feed at shoulder level and “bend over” to do so. The ‘necks for sex’ idea also doesn’t work alone because it doesn’t explain why female giraffes have long necks since they don’t engage in battles for mating.

This returns us to a common theme of evolutionary biology. Evolution is “survival of the fit enough,” more so than “survival of the fittest.” It doesn’t require perfection. Many organisms with varying traits are able to survive and reproduce, and this perhaps leads to the beautifully diversity we see today. The giraffe may not be the perfect organism, but the giraffe is the perfect giraffe.

Check out some of the recent research on Giraffe Necks:

Badlangana, N. L., Justin W. Adams, and Paul R. Manger. 2009. The Giraffe (Giraffa Camelopardalis) Cervical Vertebral Column: A Heuristic Example in Understanding Evolutionary Processes? Zoological Journal Of The Linnean Society 155.3: 736-57.

Mitchell, G., S. J. Van Sittert, and J. D. Skinner. 2009. Sexual Selection Is Not the Origin of Long Necks in Giraffes. Journal of Zoology 278.4: 281-286.

Simmons, R. E., and R. Altwegg. 2010. Necks-for-sex or Competing Browsers? A Critique of Ideas on the Evolution of Giraffe. Journal of Zoology 282.1: 6-12.

Simmons, Robert E., and Lue Scheepers. 1996. Winning by a Neck: Sexual Selection in the Evolution of Giraffe. The American Naturalist 148.5 : 771-786.

Solounias, N. 1999. The Remarkable Anatomy of the Giraffe’s Neck. Journal of Zoology 247.2: 257-268.

Taylor, M. P., D. W. E. Hone, M. J. Wedel, and D. Naish. 2011. The Long Necks of Sauropods Did Not Evolve Primarily through Sexual Selection. Journal of Zoology 285.2 : 150-161.

Wilkinson, David M., and Graeme D. Ruxton. 2011. Understanding Selection for Long Necks in Different Taxa. Biological Reviews: 616-630.

Rise of Antibiotic Resistance

Contributed by Richard Parilla

In 1928 a discovery made by Scottish scientist Alexander Fleming would change modern medicine. Fleming observed that the fungus Penicillium was able to kill disease causing pathogens. This discovery won Fleming a Nobel Prize in 1945 and led to development of antibiotics. The effectiveness of these drugs, once referred to as “miracle drugs”, led them to become used very regularly to treat a variety of illnesses. However, these lifesaving antibiotics have become far less effective due to the increasingly more common bacterial strains that are antibiotic resistant.

Antibiotics function by either directly killing bacteria themselves or by inhibiting their growth and reproduction. So how does bacterial strains resistance to certain antibiotics come about? Well an easy way to think about this is in evolutionary terms. The use of antibiotics selects for bacterial strains that are resistant to the mechanism by which the antibiotic targets the pathogen. Since all the non-resistant bacteria are wiped out by the antibiotic, only the resistant bacteria can reproduce and spread. This is an interesting perspective since it shows that humans can have an impact on the evolution of a species through implementation of novel selective pressures such as antibiotics.

Over the past decade antibiotic resistance has become a very threatening problem to society. It is has been a topic which has continually made headlines over the past few years. Why has the threat of antibiotic resistant microbes risen? The World Health Organization points to the misuse of antibiotics and over prescription as the cause of the accelerated emergence of the resistant bacteria strains. Due to the nature of this problem it would seem that it will be a frequent topic of discussion in the near future.

For Further Further Reading:

“Antimicrobial Resistance.” WHO. N.p., May 2013. Web. 20 Apr. 2014.

Austin, D. J. “The Relationship between the Volume of Antimicrobial Consumption in Human Communities and the Frequency of Resistance.” Proceedings of the National Academy of Sciences 96.3 (1999): 1152-156. Print.

Bonhoeffer, S. “Evaluating Treatment Protocols to Prevent Antibiotic Resistance.” Proceedings of the National Academy of Sciences 94.22 (1997): 12106-2111. Print.
Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 16 Sept. 2013. Web. 20 Apr. 2014.

“General Background: About Antibiotic Resistance.” Tufts University. N.p., n.d. Web. 20 Apr. 2014.

Hampton, L. M., M. M. Farley, W. Schaffner, A. Thomas, A. Reingold, L. H. Harrison, R. Lynfield, N. M. Bennett, S. Petit, K. Gershman, J. Baumbach, B. Beall, J. Jorgensen, A. Glennen, E. R. Zell, and M. Moore. “Prevention of Antibiotic-Nonsusceptible Streptococcus Pneumoniae With Conjugate Vaccines.”Journal of Infectious Diseases 205.3 (2012): 401-11. Print.

Levy, Stuart B. “The Challenge of Antibiotic Resistance.” Diss. Texas U, 1998. Web.

Lupo, Agnese, Sébastien Coyne, and Thomas Ulrich Berendonk. “Origin and Evolution of Antibiotic Resistance: The Common Mechanisms of Emergence and Spread in Water Bodies.” Frontiers in Microbiology 3 (2012): n. pag. Print.

Stöppler, Melissa C., M.D. “Antibiotics 101 –” MedicineNet. N.p., 3 Sept. 2012. Web. 20 Apr. 2014.

Woodford, Neil, Jane F. Turton, and David M. Livermore. “Multiresistant Gram-negative Bacteria: The Role of High-risk Clones in the Dissemination of Antibiotic Resistance.” FEMS Microbiology Reviews 35.5 (2011): 736-55. Print.

HIV/AIDS and the Evolution of Drug Resistance

Contributed by June Tzu-Yu Liu, Akanksha Samal and Amy Jeng

“Currently, the CDC estimates that more than 1.1 million people in the United States are living with HIV infection and around 180,900 people are unaware that they are infected. It has been observed that people diagnosed with HIV are increasing annually, around 50,000 new incidences per year.”  –

What is HIV? What is AIDS?

HIV (Human Immunodeficiency Virus) is a retrovirus that attacks the human immune system, more specifically, CD4+ T cells. These cells are essential components of the body’s defense system against infections and diseases. HIV invades T cells, uses them for replication and destroys them. The terms HIV and AIDS are often used interchangeably, however there is an important distinction. HIV is the name of the retrovirus that invades cells, while AIDS (Acquired Immunodeficiency Syndrome) is the most advanced stage of the HIV infection. People with healthy immune systems are able to fight off infections, however, people with HIV have compromised immune systems and are highly susceptible to opportunistic infections. Opportunistic infections refer to infections that do not cause serious health threats in healthy individuals, but cause life threatening illnesses in HIV positive individuals.

How does HIV replicate?

HIV mainly targets the T CD4+ cells in our bodies. When HIV enters the host, it binds to receptors on the surface of T cells. It is analogous to using a key to unlock a door. If the HIV has the right key, it can fuse with the T cell and release its genetic material into the cell. The genetic material in HIV is RNA, thus it must change its genetic material into DNA so that the host cell can replicate the genetic material. An enzyme called reverse transcriptase changes RNA into DNA. The virus’ genetic material can now integrate with the host’s. The host cell will unknowingly replicate the virus’ genetic material. Then, the virus will push itself out of the host cell, killing it in the process.

Drug Resistance?

There is high genetic diversity in HIV because of its rapid replication and high mutation rate. Currently, doctors are using a combination of different antiretroviral drugs to inhibit various steps in the HIV life cycle, leading to a synergistic effect. One major drawback to this approach, however, is drug resistance.  Scientists have found that using antiretroviral therapy (ART) increases the rate of drug resistance. According to a case study from China, prevalence of drug-resistant variants in therapy patients increased significantly to 45.4% in three months and 62.7% in six months. Alarmingly, drug resistant variants can replace the wild type variants completely within 14-28 days of treatment. Similar results were found in a case study in South Africa in which a large percentage of patients who did not respond to treatment harbor viruses with drug-resistance mutations. The effectiveness of therapeutic regimens to control the HIV pandemic are compromised due to drug resistance.

A common misconception is that evolution is a chance event. Evolution of HIV is not a chance event; it is driven by drug selective pressures. Also, organisms are commonly perceived as  getting “better” through evolution. The HIV virus isn’t getting better. It’s becoming more adapted to it’s environment. Resistant HIV is not “better” than the non-resistant strains. They have just evolved to be better suited for their environment.

For more information please see the following papers:

Hegreness, M. et al. 2008. Accelerated evolution of resistance in multidrug environments. Proceedings of the National Academy of Sciences of the United States of America 105 (37): 13977-13981.

Li, J.Y., et al. 2005. Prevalence and evolution of drug resistance HIV-1 Variants in Henan, China. Cell Research 15: 843–849.

Mammano, F., et al. 2000. Retracing the Evolutionary Pathways of Human Immunodeficiency Virus Type 1 Resistance to Protease Inhibitors: Virus Fitness in the Absence and in the Presence of Drug. Journal of Virology 74 (18): 8524-8531.

Mansky, L. M. 2002. HIV mutagenesis and the evolution of antiretroviral drug resistance. Drug Resistance Updates 5 (6), 219-223.

Marconi, V.C. et al. 2008. Prevalence of HIV-1 Drug Resistance after Failure of a First Highly Active Antiretroviral Therapy Regimen in KwaZulu Natal, South Africa. Clinical Infectious Diseases 46: 1589-1597.

Peeters, M., et al. 2002. Risk to Human Health from a Plethora of Simian Immunodeficiency Viruses in Primate Bushmeat. Emerging Infectious Disease 8: 451-457.

Sarkar, I., et al. 2007. HIV-1 Proviral DNA Excision Using an Evolved Recombinase. Science 316: 1912-1915.

Smith, R. J., et al. 2010. Evolutionary Dynamics of Complex Networks of HIV Drug-Resistant Strains: The Case of San Francisco. Science 327: 697–701.


The Evolution of Helping in Nature

You would share a cookie, but why would a meerkat?

Contributed by Jessica Etienne, Kavya Reddy, Madison Malone, Okeoghene Ogaga

Evolution, the inherited change in a group of organisms over time, is often misunderstood. One major misconception is that evolution leads to immoral behavior. However, many animals, insects and plants have evolved altruistic behavior, an interaction between two individuals in which one individual reduces its own fitness (the ability of an individual to survive and reproduce) for the benefit of another. In other words, the individual is doing something good for someone else. Altruism is important evolutionarily because it interacts with natural selection by promoting cooperation of a group as a method of competition against others. Altruism can come in two forms: either an organism performs an action without anything in return or an organism becomes less competitive with other individuals without receiving any benefits. It seems counter intuitive for organisms in nature to perform a selfless action, however a chimpanzee will help another without receiving anything in return. One idea as to why this happens is that it has evolved due to indirect fitness. The total fitness of an individual includes indirect and direct fitness; indirect fitness is benefit for oneself gained through the fitness of others, while direct fitness is the benefit gained directly from one’s own actions. Contrary to what many believe, the fittest individuals are the ones that manage to spread their genes the most because fitness incorporates more than an individual’s physical capabilities.

Typically within a population, organisms tend to help those that are related to them rather than strangers; for example, plants will compete less for resources when they are next to their relatives than when they are next to strangers. This is most likely because individuals that are related to one another share a percentage of DNA. A unit for expressing this percentage is called coefficient of relatedness (r). One can model the likelihood of altruistic behavior using relatedness and Hamilton’s Rule, which states that the coefficient of relatedness, multiplied by the benefit (b) that the related individual receives, should be greater than the cost (c) that the individual performing the action experiences:  rb-c>0  or rb>c

Despite the accuracy of Hamilton’s Rule in predicting the evolution of altruistic behavior, it is important to remember that it a model that describes why altruism occurs, and is still being investigated. For more on Hamilton’s rule, see the video below.

In order for organisms to show altruism preferentially towards related individuals, they need to be able to know who they are related to; organisms do this two different ways, either using kin recognition (they can recognize who their brothers are) or kin fidelity (families stay together).

In addition, altruistic behavior does not imply that an individual will sacrifice itself for the “good of the species,” but rather Individuals are sacrificing themselves to increase the fitness of their relatives, and therefore increase their own fitness indirectly.

For more information, go to:

Abbot, P., Abe, J., Alcock, J., Alizon, S., Alpedrinha, J. A. C., Andersson, M., Andre, J.-B., et al. (2011). Inclusive fitness theory and eusociality. Nature, 471(7339), E1–E4. doi:10.1038/nature09831

Curry, O., Roberts, S. G. B. and Dunbar, R. I. M. (2013), Altruism in social networks: Evidence for a ‘kinship premium’. British Journal of Psychology, 104: 283–295. doi: 10.1111/j.2044-8295.2012.02119.x

Dudley, S., Murphy, G., and File, A. 2013. Kin recognition and competition in plants. Functional Ecology 27(4) 898-906. DOI: 10.1111/1365-2435.12121

Ratnieks, F. and Wenseleers, T. 2008. Altruism in insect societies and beyond: voluntary or enforced? Trends in Ecology and Evolution 23(1) 45-52. doi:10.1016/j.tree.2007.09.013

Yamamoto, S., Humle, T., and Tanaka, M. 2012. Chimpanzees’ flexible targeted helping based on an understanding of conspecifics’ goals PNAS 109 (9) 3588-3592. doi:10.1073/pnas.1108517109

Got Lactase?

Contributed by Seth Appiah-Opoku, Judy Chen, and Steven Sun

Do you know anybody who is lactose intolerant? Today, about one-third of people in the world are unable to digest lactose, milk sugar. It is likely that before the agricultural revolution, most people were lactose intolerant. After populations began to raise cattle rather than search for their food on a daily basis, people had more access to milk, a luxury that was previously only consumed when they were infants. On the chance that food became rare, individuals who were able to digest lactose—lactose persistent individuals—were more likely to survive because they could consume milk instead. Because they were more likely to survive, these people were also more likely to have children, passing on their ability to digest lactose, and therefore increasing the presence of this ability in the population.

According to current research on the topic, the genetic mutation that causes lactose persistence appeared first in the Arabian Peninsula and Middle East around 6,000 to 2,000 years ago before spreading to northern Africa. Around that similar time, the domestication of cattle was already established in northern Africa. Within Africa, cattle domestication further spread from the Sahara to Sudan and northern Kenya about 4,500 years ago. Then, about 3,300 years ago, cattle domestication continued to spread into southern Kenya and northern Tanzania. Following a similar time scheme, the Arab expansion led to an increased mixing of different populations, and the lactose persistence gene was introduced into eastern Africa within the last 1,400 years. Ultimately, lactose persistence spread to southern Africa within the last 1,000 years.

Further research is being conducted; however there is strong evidence that because lactose persistence and the domestication of cattle arose around the same time in similar areas, it is likely that the development of lactose persistence was a result of cattle domestication.

To read the paper behind this information, check out:

Ranciaro, A., Campbell, M. C., Hirbo, J. B., Ko, W., Froment, A., Anagnostou, P., … Tishkoff, S. A. (2013). Genetic origins of lactase persistence and the spread of pastoralism in africa. American Journal of Human Genetics, 94, 1-15.

Evolution: A Quest for Change

Contributed by Mark Jedrzejczak

Ever since Morgan Freeman’s success on the Science network’s program, “Through the Wormhole” the actor has been much sought out for his iconic narrative voice and style. We are proud to present the first episode of his* most recent documentary series on the topic of macroevolution, “Evolution: A Quest for Change”.

(* well, someone that sound like him, anyway.)

The title reflects a little tongue-in-cheek on the part of the producers, since evolution is not really a quest, since quests involve a mission with an end goal. Instead, evolution is more like a knight going doing a bunch of random missions and after some time, he starts to choose those missions that get him the most princesses. Similarly, evolution is a process driven by the nonrandom selection of heritable traits that impart the best fitness. This ends up changing the gene frequencies in a population over time. On a macroscopic level, this is characterized by the evolution of a species’ gene pool as a whole, often leading to divergence and speciation. The process of macroevolution is responsible for the existence of all the organisms that ever were and will be inhabiting our pale-blue dot, planet Earth.

This documentary presents the topic of large-scale evolution, the main mechanisms that drive macro evolution, and what evidence exists for the process. At the same time, the documentary helps highlight the importance of scientific literacy, critical thinking, and smart science teaching, especially for today’s youth. Research done by Hayat Hokayem and Saouma BouJaoude (2008) on college student’s perception of evolution underscores the importance of understanding the student’s perspectives on the theory of evolution. In addition, their research suggests that accepting and working with an individual’s “cultural milieu” or worldview is the most effective method of conveying scientific ideas. An instructor simply handing a student a stack of scientific information is not good enough, especially when the latter starts reading the information with a set of presuppositions. These biases should to be understood and used as building blocks, and should not be seen as pieces that instructors need to be tear down.

A more effective way of teaching is to build upon student’s misconceptions…and also not to even use the word misconception. One study by April Cordero Maskiewicz and Jennifer Evarts Lineback (2013) advocates using students’ incorrect ideas about science as a resource for refining teaching strategies.

This documentary addresses a few of these “misconceptions”, especially a couple that were highlighted in the Maskiewicz and Lineback study. These were that ‘natural selection is trying to give what the organisms need.’ The video clearly discusses that evolution and the process of natural section have no goal or “finish line.” Another incorrect idea, taken from the “MiTEP List of Common Geoscience Misconceptions Organized by the Earth Science Literacy Principles”, that biases new students in the field of evolutionary biology, is the “young Earth” model, and this too is addressed in the video.

For more information, see:

Age of the Earth. U.S. Geological Survey. 1997. Archived from the original on 23     December 2005. Retrieved 2006-01-10.

Oberthür, T, Davis, DW, Blenkinsop, TG, Hoehndorf, A (2002). Precise U–Pb mineral ages, Rb–Sr and Sm–Nd systematics for the Great Dyke, Zimbabwe—constraints on late Archean events in the Zimbabwe craton and Limpopo belt. Precambrian Research 113 (3-4): 293–306.

Carlin, J. L. (2011) Mutations Are the Raw Materials of Evolution. Nature Education Knowledge 3(10):10.

H Su, L-J Qu, K He, Z Zhang, J Wang, Z Chen and H Gu. (2003) The Great Wall of China: a physical barrier to gene flow? Heredity. 90, 212–219.

Liman, R., Sheehy, B. & Schultz, J. (2008) Genetic Drift and Effective Population Size. Nature Education 1(3):3.

Macroevolution. Understanding Evolution. 2014. University of California Museum of Paleontology.

Hokayem, H. and BouJaoude, S. (2008), College students’ perceptions of the theory of evolution. J. Res. Sci. Teach., 45: 395–419.

April Cordero Maskiewicz and Jennifer Evarts Lineback Misconceptions Are “So Yesterday!” CBE Life Sci Educ September 4, 2013 12:352-356.

MiTEP List of Common Geoscience Misconceptions Organized by the Earth Science Literacy Principles.

Survival of the Fittest: Monarch and Viceroy Butterflies

By: Chris Frey, Griffin Murphy, Jason Shah, Mick McColl

Darwin’s Theory of Evolution was a groundbreaking advancement, explaining how natural selection results in the inherited biological change within a population. This is evolution. Biological fitness is central to this theory, and although many people understand that the fittest survive, not all understand what this truly means.  Biological fitness is measured by the ability of an organism to reproduce and successfully pass on its genes to future generations. Misconceptions arise when individuals perceive the largest, strongest organisms within a population to be the most biologically fit. To demonstrate fitness in the context of evolution, one need only look at butterflies.  They come in all shapes, sizes and colors, sometimes adopting another species’ physical characteristics in a process known as mimicry.  Mimicry comes in several varieties, including Batesian mimicry, which is when a palatable organism mimics a species that is unpalatable to predators. Consequently, they are avoided by predators, increasing their fitness.

A vivid example of Batesian mimicry is depicted by Viceroy and Monarch Butterflies. Monarch butterflies are unpalatable due to toxic milkweeds they consume as larvae, which results in low levels of predation in their natural environment.  Viceroy butterflies have wings emblazoned with similar shape and color schemes, ostensibly reducing the predation rate. Colors must be matched very closely as avian predators have some of the most developed eyes in the animal kingdom (for more information, see paper from 2012 by Stoddard and colleagues listed below).

A vivid example of Batesian mimicry is depicted by Viceroy and Monarch Butterflies. Monarch butterflies are unpalatable due to milkweed they consume as larvae, which results in low levels of predation in their natural environment.  Viceroy butterflies have wings emblazoned with similar color schemes, ostensibly reducing the predation rate. Wing shape plays an important role in mimicry too (for more information, see paper from 2013 by Jones and colleagues listed below).

Monarch and Viceroy butterflies serve as a model organism for mimicry and the evolutionary concept of survival of the fitness. Similar mimicry models have been recently exposed within a microbiological context. A bacterial pathogen has been discovered that mimics the structure of some of its intended hosts’ carbohydrates. This structural mirroring results in a reduced innate immune response by the host (for more information, see paper from 2009 by Carlin and colleagues listed below). In essence, the bacterium mimics the structure of the host species in order avoid immune detection and thus increase its chance of survival.

A visual explanation of Monarch and Viceroy mimicry has been provided below:


In addition, listed below are some articles on mimicry

Carlin, Aaron, et, al. 2009. Molecular mimicry of host sialylated glycans allows a bacteria pathogen to engage neutrophil Siglec-9 and dampen the innate immune response. Blood Journal. 2009.

Holmes, B. 2010. Accidental evolution: the real origin of species. New Scientist 205: 30-33.

Jones, R.T. 2013. Wing shape variation associated with mimicry in butterflies.        Evolution 67: 2323-2334.

Matthews, E.G.  1977. Signal-Based frequency-dependent defense      strategies and the evolution of mimicry. The American Naturalist 111: 213-222.

Rowe, C. C. Halpin. 2013. Why are warning displays multimodal. Behavioral Ecology and Sociobiology 67: 1425-1439.

Stoddard, M.C. 2012. Mimicry and masquerade from the avian visual perspective. Current Zoology 58: 630-648.

Williamson B.G., C.E. Nelson. 1972. Fitness set analysis of mimetic adaptive strategies. The American Naturalist 106: 525-535.

Yahner, R.H. 2012. Additional adaptations against predation. Wildlife Behavior and Conservation 55-64.


Convergent Evolution

Contributed by Greg Fricker and Geoffrey Welch

Have you ever thought how similar butterflies and bats are in taking to the skies? Looking around, we see that both of these creatures use wings for flight; however, butterflies are insects, and bats are mammals, like you and me. If we imagine the tree of life, these organisms would be on distant branches, having distinct lineages, but they have similar characters. Convergent evolution is this phenomenon where similar characters evolve independently in multiple lineages. This seems like a counter-intuitive process initially, as similar features are often associated with relatedness. As evolution is all about favorable hereditary traits being passed on to future generations, how then do the same traits arise in completely separate lineages?

The answer lies in the selection pressures organisms face. When a certain trait is so remarkably important for organisms in a particular environment, it can be expected to arise in multiple different species. For example, consider underwater foraging birds. Cormorants, penguins, puffins, and gannets, each with minimal relatedness to the others, have evolved to have a “pygostyle” tail, which is straight and elongated.  This pygostyle tail is vitally important to these birds, as it acts like a “rudder,” allowing for enhanced steering in water, just like the rudder on a sailboat. This rudder is so beneficial for these underwater foraging birds in finding food–and thus surviving and having offspring–that we see it arise multiple times. When the random mutations occurred separately in these four species, the advantage provided by this “rudder” tail ensured that the pygostyle phenotype would be passed along to future generations.

Yet another example can be seen in echolocation, or the ability of an animal to use vocalizations to locate objects and better “see” its environment.  It might be easy to dismiss instances of convergence within the birds previously stated due to the fact that all four cases are aquatic birds, and thus seem as though they would be at least somewhat related. In that case, consider bats and dolphins. Despite the fact that they are both mammals, bats and dolphins would be expected to share little in common, as they both evolved in drastically different environments.  However, both utilize echolocation. Not only did they both evolve the same physical trait, but it has been determined that the two groups converged on a genetic level as well. Three separate genes that play a role in echolocation, including a protein associated with inner ear hair formation, have been shown to have converged among three separate groups–dolphins and two groups of bats. Echolocation provided such a substantial fitness benefit in the two separate environments of caves and marine life that natural selection drove the evolution of it in these rather unrelated lineages.

For more information, check out the video below:

Also, check out some of the recent research on convergence:

Parker et al. 2013. Genome-wide signatures of convergent evolution in echolocation mammals.  Nature. 502: 228-231.

Shen et al. 2012. Parallel evolution of auditory genes for echolocation in bats and toothed whales.  PLoS Genetics.  8(6): e1002788.

Liu et al. 2010. Convergent sequence evolution between echolocating bats and dolphins. Current Biology. 20 (2): 53-54.

Jones, G and MW Holderied.  2007.  Bat echolocation calls: adaptation and convergent evolution.  Proceedings of the Royal Society B. 274: 905-912.

Felice, RN and PM O’Connor. 2014. Ecology and caudal skeletal morphology in birds: the convergent evolution of pygostyle shape in underwater foraging taxa. PLoS One.  9(2): e89737.

Alerstam et al. 2011. Convergent patterns of long-distance nocturnal migration in noctuid moths and passerine birds. Proceedings of the Royal Society B. 278(1721): 3074-3080.

Gleiss et al. 2011.  Convergent evolution in locomotory patterns of flying and swimming animals.  Nature Communications. 2: 352.