A Pain in the Neck: Costs of Natural Selection in Giraffes

Contributed by George Yang, Carl Dalmeus, and Alan Kwan

“Survival of the fittest”. The saying is used everywhere – in sports, academics, commercials, and other cultural norms. Society paints the image that the most successful people are at their physical and mental peak and have been that way since the beginning. So when survival of the fittest is mentioned in evolutionary science, many people make the common mistake of believing the fastest, biggest, and strongest organisms are the ones that survive in nature. Instead, fitness is the ability for an organism to not only survive in its environment but also successfully reproduce in the future. When facing natural selection, species may find that maintaining large morphological structures may not be the evolutionarily beneficial decision.

When people hear about giraffes, one of the first things they think of is probably their necks. Giraffes are the tallest living land animals on the planet and well-known for their long necks that stretch high over the savannas of Africa. But why exactly are the necks of giraffes so long? The most common explanation that dates back to as early as the start of the 19th century is that giraffes use their long necks to help them browse above the canopy for vegetation, which gives them an advantage over members of the same and different species. Later research found other explanations such as sexual selection (male-male combat and attracting female giraffes), increased vigilance (able to see predators from further away), and thermoregulation (increased surface area allows for greater cooling ability). For more information on a few of these hypotheses, see another recent post.

However, there are also costs associated with the long necks of giraffes. Despite having long necks, giraffes actually reach optimal feeding when their necks are bent and have the tendency to feed from low shrubs particularly during dry seasons. Longer necks would also result in enlargement of the heart, thickening of the artery walls, and higher blood pressure in order to push blood into the brain. Therefore, maintaining longer necks may be an unnecessary expenditure of energy. In addition, research suggests that giraffes with longer necks stick out from the crowd and are more likely to be subject to predation.

The long necks of giraffes is just one of many examples in nature illustrating that there are costs and benefits to most adaptations. The idea that natural selection produces perfect organisms with perfectly advantageous adaptations is just a tall tale.

For more information about the costs of selection in giraffes and other organisms, please refer to the below articles:

Cameron, E.Z. & J.T. du Troit. 2007. Winning by a neck: tall giraffes avoid competing with shorter browsers. American Naturalist 169: 130-135.

Englemoer, D.J.P., Donaldson, I., & D.E. Rozen. 2013. Conservative Sex and the Benefits of Transformation in Streptococcus pneumoniae. PLoS Pathogens 9.

Kusche, H. & A. Meyer. 2014. One cost of being gold: selective predation and implications for the maintenance of the Midas cichlid colour polymorphism (Perciformes: Cichlidae). Biological Journal of the Linnean Society 111: 350-358.

Liker, A. & T. Szekely. 2005. Mortality costs of sexual selection and parental care in natural populations of birds. Evolution 59: 890-897.

Mougeotf, F. & V. Bretagnollef. 2000. Predation as a cost of sexual communication in nocturnal seabirds: an experimental approach using acoustic signals. Animal Behavior 60: 647–656.

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

Wilkinson, D.M. & G.D. Ruxton. 2012. Understanding selection for long necks in different taxa. Biological Reviews 87: 616-630.

The Evolutionary Significance of the Narwhal’s “Tusk”

Contributed by Madeline Haley and Melissa Querrey

First, a short introduction to narwhals by yours truly.


The narwhal, or Monodon monoceros, is a cetacean mammal that inhabits the Arctic waters and is most commonly recognized for its large “tusk”, which closely resembles the horn of the mythical unicorn. Contrary to popular belief, this “tusk” is actually a modified tooth that forms during development from a pair of tooth buds and projects outward from the maxilla, or upper jaw. While both males and females can grow tusks, males tend to have tusks more often than females.

There has been much debate among researchers about the true function of the narwhal’s tusk. It was initially thought that the tusk was only used as an evolutionary means of self-defense and breaking the ice that covers the surface of their aquatic habitats so breaths of air can be taken. However, recent study of the anatomy of the tusk by Nweeia and colleagues revealed nerves that lead directly to the brain, giving evidence of its additional function as a sensory organ.This sensory feature serves several purposes to the narwhal by detecting changes in the external environment, such as salinity and temperature. Because these functions of the narwhal’s tusk increase its chances of survival and are retained in the population, it can be said that they are a result of natural selection.

Additionally, secondary functions of the tusk have developed due to sexual selection, which have facilitated the tusk’s persistence. Based on the discovery of broken tusk fragments and scarring, it can be inferred that male narwhals use their tusk in an aggressive fashion in order to assert sexual dominance and eventually find a mate.

While the narwhal’s tusk may seem like an obnoxious physical display, it is clear that evolutionary forces of both natural and sexual selection have driven the species to utilize its tusk in a way that enables its survival and overall individual and reproductive fitness.

Finally, check out this awesome video about narwhals.

And, for more information:

Palsboll, P.J, Heide-Jorgensen, M.P, & R. Dietz. 1997. Population structure and seasonal movements of narwhals, Monodon monoceros, determined from mtDNA analysis. Heredity 78: 285-292.

Nweeia, M. T., Eichmiller, F. C., Hauschka, P. V., Donahue, G. A., Orr, J. R., Ferguson, S. H., Watt, C. A., Mead, J. G., Potter, C. W., Dietz, R., Giuseppetti, A. A., Black, S. R., Trachtenberg, A. J., & Kuo, W. P. 2014. Sensory ability in the narwhal tooth organ system. The Anatomical Record, 297: 599–617.

Nweeia, M.T., et al. 2009. Considerations of anatomy, morphology, evolution, and function for narwhal dentition. The Anatomical Record 295, 6: 1006-1016.

Silverman, H. B., & M. J. Dunbar. 1980. Aggressive tusk use by the narwhal (Monodon monoceros L.). Nature 284.5751: 57-58.

Brear, K., et al. 1993. The mechanical design of the tusk of the narwhal (Monodon nonoceros: Cetacea). Journal of Zoology 230.3: 411-423.

Mirceta, S., Signore, A.V., Burns, J.M., Cossins, A.R., Campbell, K.L., & Berenbrink, M. 2013. Evolution of Mammalian Diving Capacity Traced by Myoglobin Net Surface Charge. Science 14: 1234192

“Narwhals.” Narwhals. National Geographic, n.d. Web. 18 Apr. 2014.<http://video.nationalgeographic.com/video/narwhals?source=relatedvideo>.



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.com.” 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.”  – aids.gov

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.


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. http://mitep.mspnet.org/media/data/MiTEP_List_of_Common_Geoscience_Misconceptions.pdf?media_000000007297.pdf

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.