Can we decide the direction of evolution?

Contributed by Ina Huang, Jenny Huang

Many people believe that natural selection subjectively selects the favorable traits in a population. But in fact, it is a passive process that does not involve organisms “trying” to adapt. Natural selection can be influenced by many factors, one of which is the random mutations that may occur. These mutations can range from those that influence the color adaptations we see in animals like the rat snake (Pantherophis obsoletus) to sickle cell disease in humans. Under different environmental conditions, some mutations lead to a higher survival rate of individuals and are therefore passed onto the next generation. This concept of the organism becoming more suited to its current environment is roughly the basis of adaptive evolution. This is a fundamental principle for natural selection instead of specific desires of species.

The generation of mutations in organisms is random. Nevertheless, there are attempts to comprehend the process of mutations. One emerging area of evolutionary biology that does this is called quantum biology. In quantum biology, the principle idea is that the interactions and movements of protons within the genome have a major influence on the entire organism. It is theorized that whether a mutation occurs or not in a gene is due to the position of a proton on that gene. The movement of such a small and basic component in DNA is able to generate drastic changes. It is speculated that shifts in the proton occur when the organism is exposed to selective conditions in their environment. These environmental factors induce selective pressures on the organism genes. Essentially, this means that at the level of the organism’s DNA, specific genes are placed under pressure. It is these pressures that provide the conditions that can induce mutation. First, it should be noted that whether or not the mutation occurs is random. However, like the organisms themselves, the protons at the atomic level are in constant motion. Thus mutations may arise at anytime.

e.coli cartoonLet’s consider this idea with a simplified example using a strain of Escherichia coli that is nonfermenting. This means that this strain cannot use anaerobic respiration to obtain energy. If E.coli is grown on plates that are rich in lactose, a nutrient for growth, it has been shown that some colonies will develop a mutation that allows them to ferment or metabolize energy from lactose.  So for those E.coli colonies on lactose-rich plates, to take advantage of the resources in their environment, a beneficial mutation can spontaneously occur that allows them to metabolize lactose. As mentioned previously, these mutations are random. They bacteria cannot force or influence themselves in anyway to gain the lactose-fermenting mutation. For the E. coli colonies that are able to utilize lactose and metabolize it, they are referred to as lac+. The strain that does not ferment on lactose-rich plates will be referred to as lac-.

proton shift

This figure shows a massive oversimplification of the atomic level in DNA. When the proton shifts the surroundings are also affected. This change is capable of forming the mutated gene.

Now, assume that there is a specific gene that controls the ability to ferment in E. coli. Like everything else on Earth, that gene is made up of protons, electrons, and neutrons at the atomic level. Let’s focus on one proton for now.  If the proton is in shape A (AKA “configuration” in scientific language) then the E.coli is the wild type lac- , but if that proton shifts then it is lac+. The main idea is that the mutation in yeast is due to the change in the position of this one proton. Apparently, when the proton shifts this particular gene is pushed toward its mutated state. Though whether this shift occurs or not at some time period is random. When the environmental condition is providing some selective factor onto the genes of the organism the proton enters a state of decoherence, or instability. In this state the gene either crosses the line to become its mutated version or stays in the wild type form.


This images summaries that when E.coli is plated on lactose rich plates a greater percentage of the colonies become lac+. On the other hand, in the plates lacking lactose the occurrence of the lac+ mutation is less likely to occur.

Adaptive evolution is an interesting concept because it challenges the idea that mutations are completely random. As it is shown in the E. coli example, the environment impacted the gene under selection. The interactions with the environment in the example, allowed for the selection of lac+ E. coli. However, this does not mean that the organisms themselves have the abilities to influence which mutations may or may not arise. While, selective factors may direct the path of mutations in organisms, it does not induce  the mutations. Individuals have no control over the formation of mutations. This area of adaptive mutation and the application of quantum biology is still relatively young. However, researching these two concepts provides more information on the evolutionary process.


Video Resource:

To learn more about how quantum biology relates to evolutionary biology watch the TEDtalk given by Jim Al-Khalili.


Reading resources for further information:

Bershtein, S., and D. S. Tawfik. 2008. ‘Ohno’s model revisited: measuring the frequency of potentially adaptive mutations under various mutational drifts’, Molecular Biology Evolution, 25: 2311-8.

Gerstein, A. C., D. S. Lo, and S. P. Otto. 2012. ‘Parallel genetic changes and nonparallel gene-environment interactions characterize the evolution of drug resistance in yeast’, Genetics, 192: 241-52.

Levin, B. R., and O. E. Cornejo. 2009. ‘The population and evolutionary dynamics of homologous gene recombination in bacterial populations’, PLoS Genet, 5: e1000601.

Lynch, M., and A. Abegg. 2010. ‘The rate of establishment of complex adaptations’, Molecular Biology Evolution 27: 1404-14.

McFadden, J., and J. Al-Khalili. 1999. ‘A quantum mechanical model of adaptive mutation’, Biosystems, 50: 203-11.

Ogryzko, V. 2009. ‘On two quantum approaches to adaptive mutations in bacteria’, NeuroQuantology, 7:564-595.

Dolphin’s New Hunting Tool: Humans

Contributed by Brian Lee

Researchers and scientists that have studied the Bottlenose dolphins (Tursiops truncatus) have found a new phenomenon regarding these dolphins: dolphins now use humans to get their food!

As dolphins are known to be one of the more intelligent species with complex cognitive and sophisticated learning abilities, it comes as no surprise that dolphins living in close proximity to human civilization have learned to utilize their resources and surroundings, one of which is human resources.

Examples of this phenomenon include: tailing fishing boats and picking up discarded fishes, visiting fish farms set up for commercial use, and begging directly to humans! In Savannah, Georgia, dolphins were observed to be begging significantly more when fishermen were cleaning and prepping for their next fishing escapade.


Dolphins observed to be begging in ports near Savannah, Georgia



Dolphins tailing fishing boats and feeding off of the discarded pile of fishes

Of course, there are no free lunches in life. In Laguna, Brazil, dolphins and fishermen have a cooperative relationship in achieving the same goal: catching fish. The dolphins will drive a school of fish toward the fishermen and even give off a signal of a tail or head slap to the fishermen indicating when to throw nets out. In exchange for helping out, the fishermen will give their discards to the dolphins. It’s a win-win situation!


Cooperative task between fishermen and dolphins in Laguna

These phenomena could be attributed to social learning from older dolphins and inter-generational information transfer. Evidence has been shown that dolphins were able to learn complex behaviors in Shark Bay, Western Australia. However, the maintenance of these behaviors could be a collective result of social learning, genetics, and ecology.

Natural selection is about how well species are able to survive and adapt in a particular environment. While dolphin’s populations could evolve new methods for catching fish that do not involve humans or could evolve new limbs making it easier to grab fish, they instead learned and adapted to the growing technology of humans. It might be a lazier option, but in the end, the dolphins get more food either way.


For more information on this amazing phenomena, you can visit the following studies:

Cunningham-Smith, P., Colbert, D.E., Wells, R.S., Speakman, T. 2006. Evaluation of human interactions with a provisioned wild Bottlenose Dolphin (Tursiops truncatus) near Sarasota Bay, Florida, and efforts to curtail the interactions. Aquatic Mammals 32:346-356

Daura-Jorge, F.G., Cantor, M., Ingram, S.N., Lusseau, D., Simoes-Lopes, P.C. 2012. The structure of a bottlenose dolphin society is coupled to a unique foraging cooperation with artisanal fisherman. Biology Letters 8:702-705

dos Santos, M.E., Coniglione, C., Louro, S. 2007. Feeding behaviour of the bottlenose dolphin, Tursiops truncatus (Montagu, 1821) in the Sado estuary, Portugal, and a review of its prey species. Zoociencias 9:31-39

Kovacs, C., Cox, T. 2014. Quantification of interactions between common Bottlenose Dolphins (Tursiops truncatus) and a commercial shrimp trawler near Savannah, Georgia. Aquatic Mammals 40:81-94

Pennino, M.G., Mendoza, M., Pira, A., Floris, A., Rotta, A. 2013. Assessing foraging tradition in wild Bottlenose Dolphins (Tursiops truncatus). Aquatic Mammals 39:282-289

Weiss, J. 2006. Foraging habitats and associated preferential foraging specializations of Bottlenose Dolphin (Tursiops truncatus) mother-calf pairs. Aquatic Mammals 32:10-19

Evolution of Photsynthetic Sea Slugs

Contributed by Alexandria Albert and Gavon Broomfield

Bright green sea slugs that behave like plants!                                                                 Sea slugs are a diverse family of marine gastropod mollusks characterized by their soft bodies and lack of external shell. Approximately 2,300 species have been documented, all with different physical colorations that allow them to better interact with other organisms and underwater conditions. Sacoglossan sea slugs have mastered the art of kleptoplasty by extracting chloroplasts from various algal food sources and preserving them in digestive tissue, thus creating the kleptoplast. Exploring this symbiotic interaction has provided insight into multiple evolutionary processes. For example horizontal gene transfer, the transfer of genes from one species to another, in this case from the algal nucleus to sea slug cells, has facilitated the long-term use of the kleptoplasts (Cruz et al. 2013). There are still questions about the maintenance of kleptoplasts living in animal tissue, but benefits from this form of energy production have been documented.  

 E.crispate NEWE.viridis NEW

So how is it possible that sea slugs have chloroplasts? Aren’t chloroplasts only in plants?  The key to photosynthetic capable sea slugs is symbiosis. Algal nuclear genes in the sea slug digestive cells encode for chlorophyll synthesis, giving slugs green coloring, and chloroplast proteins, which later become incorporated into the slug’s DNA to get passed onto offspring. For some species of Sacoglossa, these internal or endosymbiotic chloroplasts can be maintained long-term if the slug possesses the nuclear DNA required for photosynthesis. For other species, continual feeding on algae is necessary for long-term, sustained kleptoplastic ability. Cool, right? Since the chloroplast is not native to the sea slug, important behavioral, morphological, and biochemical adaptations have evolved to maintain this symbiosis and kleptoplasty (Schwartz, Curtis, and Pierce 2014, Schmitt, Valerie, et al. 2014). 

E.timida NEW

So how do these photosynthetic sea slugs use these chloroplasts?                               Sea slugs adjust their parapodial lobes, lateral fleshy protrusions on their bodies used for movement, to manage light harvesting. When the parapodial lobes are extended, chloroplasts are exposed to direct sunlight which is then used as an energy source, a process known as phototrophy, as seen in plants. When doing this, sea slugs often resemble leaves. This leaf-like appearance aids in camouflage and avoidance of ocean-floor predators like crab, lobster, and fish (Schmitt and Wägele 2011). This unique behavioral adaptation has evolved to retain endosymbiotic chloroplasts.


Does this really work?                                                                                                   Studies have shown high levels of fitness benefits to kleptoplasty in Sacoglossa when measuring growth efficiency with trade-offs dependent upon algae diet and light exposure (Baumgartner, Pavia, and Toth 2015).  This adaptation has some limitations and may depend upon sunlight exposure and the species of algae. Too much sun exposure could cause photo-oxidative stress on kleptoplasts and decrease the rate of energy production over time (Serôdio, João et al. 2014).

For more information about the photosynthetic qualities of sea slugs, consult these sources:

  1. Baumgartner, Finn A., Henrik Pavia, and Gunilla B. Toth. “Acquired Phototrophy through Retention of Functional Chloroplasts Increases Growth Efficiency of the Sea Slug Elysia Viridis.” Ed. Erik Sotka. PLoS ONE 10.4 (2015): e0120874. PMC. Web. 6 Nov. 2015.
  2. Goodheart, J. A., Bazinet, A. L., Collins, A. G., & Cummings, M. P. (2015). Relationships within Cladobranchia (Gastropoda: Nudibranchia) based on RNA-Seq data: an initial investigation. Royal Society Open Science, 2(9), 150196.
  3. Schmitt, Valerie, and Heike Waegele. “Behavioral adaptations in relation to long-term retention of endosymbiotic chloroplasts in the sea slug Elysia timida (Opisthobranchia, Sacoglossa).” Thalassas 27.2 (2011): 226-238.
  4. Schwartz, Julie A., Nicholas E. Curtis, and Sidney K. Pierce. “FISH labeling reveals a horizontally transferred algal (Vaucheria litorea) nuclear gene on a sea slug (Elysia chlorotica) chromosome.” The Biological Bulletin 227.3 (2014): 300-312.
  5. Schmitt, Valerie, et al. “Chloroplast incorporation and long-term photosynthetic performance through the life cycle in laboratory cultures of Elysia timida (Sacoglossa, Heterobranchia).” Frontiers in zoology 11.1 (2014): 5.  
  6. Serôdio, João et al. “Photophysiology of Kleptoplasts: Photosynthetic Use of Light by Chloroplasts Living in Animal Cells.” Philosophical Transactions of the Royal Society B: Biological Sciences 369.1640 (2014): 20130242. PMC. Web. 6 Nov. 2015.

Evolution and Autism

Contributed by Suranjana Dey, Tiffany Ding, Jane Chang, Paul Nguyen

Evolution by natural selection requires the heritability of different characteristics that let some individuals produce more children, possibly because they survive longer. This might make you think that natural selection is “selecting” for traits that make individuals stronger and “better”. This isn’t necessarily true. Consider individuals suffering from autism. Individuals suffering from autism spectrum disorders (ASD) exhibit impaired social behavior, difficulty with communication, and a tendency to engage in repetitive behaviors. Evolutionary biologists are interested in how autism, which is a disorder that makes it difficult to find a mate and start a family, originated in humans. From an evolutionary perspective, a condition that decreases fertility is not expected to persist for long. However, autism continues to persist and, arguably, is arising at a faster rate.

Evolutionary biologists have honed in on one observation in particular. Autistic individuals are more likely to be males and have an interest in repetitive behaviors and mechanical actions. Men were usually the hunters in ancient hunter-gatherer societies. Hunters had to be able to predict the patterns of game movement through the seasons (a repetitive behavior), endure solitude while hunting (an antisocial state), and make and invent tools (a mechanical action). Thus, it has been hypothesized that the autistic brain is an example of an extreme male brain that initially evolved to cope with the demands of hunting. In hunter-gatherer societies, these traits allowed males to survive and provide for their families (Crespi 2013). However, these traits no longer provide the same benefits in the context of our modern world.

Evo-Bio Graphic

Another evolutionary explanation focuses on the rapid evolution of human cognition. Humans’ life histories consist of the longest period of neurodevelopment (about 25 years). Evolutionary biologists posit that autism is simply the stagnation of neurodevelopment and the persistence of a “child-like” state:

Heterochronic model for autism in regards to its restricted interests and repetitive behavior.


Developmental heterochronic model with respect to local vs. global processing in autistic individuals

This hypothesis focuses on the observation that autistic traits, such as being self-centered (averse to social interaction) and enjoying repetitive behaviors, are similar to the characteristics of a 3-year-old child. According to this hypothesis, as the genes that control life history have evolved to give humans an extended childhood, they have also become more susceptible to deleterious mutations that result in the exaggerated child-like state seen in autism (Ploeger et al., 2011). Furthermore, the AUTS2 gene has recently been implicated in the origins of ASD. In general, the AUTS2 gene appears to play a role in the rapid evolution of human cognition, which suggests the same genes that may be favorable in terms of cognition can also impact non beneficial traits (Oksenberg et al, 2013): These observations suggest that ASD could be an evolutionary by product of the rapid evolution of human cognition.

Figure 4: What happens when AUTS2 is knocked down?

For more information see:

  1. Crespi, B. 2013. Developmental heterochrony and the evolution of autistic perception, cognition and behavior. BMC Medicine 11 (119): 1-11.
  2. Ploeger, A., and Galis, F. 2011. Evolutionary approaches to autism-an overview and integration. Mcgill J Med 13 (2): 38-43.
  3. Oksenberg, N., Stevison, L., Wall, J.D., Ahituv, N. 2013. Function and Regulation of AUTS2, a Gene Implicated in Autism and Human Evolution. PLOS Genet 9 (1): 1-9.


  1. Gallup, G.G., Jr., and Hobbs, D.R.. 2011. Evolutionary medicine: Bottle feeding, birth spacing, and autism. Medical Hypothesis 77 (3): 345-46.
  2. Tordjman, S., Somogyi, E., Nathalie, C., Kermarrec, S., Cohen, D., Bronsard, G., Bonnot, O., Weismann-Arcache, C. Botbol, M., Lauth, B. 2014. Gene x Environment Interactions in Autism Spectrum Disorders: Role of Epigenetic Mechanisms. Front Psychiatry 2014 (5): 1-17.
  3. Lomelin, D.E. 2010. An Examination of Autism Spectrum Disorders in Relation to Human Evolution and Life History Theory. Nebraska Anthropologist. Paper 57: 73-81.
  4. Oksenberg, N., and Ahituv, N. 2013. The role of AUTS2 in neurodevelopment and human evolution. Trends in Genetics 29 (10): 600-608.




Penguin Adaptation to Flightlessness

Contributed by Francesca Abramson, Sydney Bunshaft, Rebecca Pankove, and Justin Elsey

Have you ever thought about why some animals fly while others swim or run? For instance, take a look at the differences at a puffin versus a penguin. Both are black and white and have a love for fish, yet a puffin can wander the skies while penguins majestically dart through the water to collect fish. This occurs because populations adapt to their environment. There are many ways this can occur such as migration, random genetic changes, or mutation, but perhaps the more fundamental method is natural selection. Evolution by natural selection is a theory that dates back to the days of Charles Darwin’s Origin of Species, which explains natural selection as a driving force of evolution that non-randomly selects for certain types of individuals that have favorable traits. This selection for favorable traits leads to higher fitness (having more offspring). This then influences the next generation’s  genotypes (genes) and phenotypes (appearance).

Natural selection, however, does not continuously select for more perfect organisms, it fluctuates just as the environment does. The change of selection pressures in the environment can either drive a population to adapt to it, leave, or perish, and penguins are a great example of this because of the trade-offs made over the course of their evolution. But we did not understand its evolutionary significance until recently.

Research done in the Department of Zoology at the University of Manitoba reveals the evolutionary origin of flightlessness in penguins, and why flight was selected against- in favor of a strong swimming ability. By comparing the energy costs of flying and diving in another wing-propelled diving bird, the thick-billed murre (Uria lomvia), scientists deduced that the energy costs of flightless diving birds is significantly lower than that of birds who can both fly and swim. Thus, it is more advantageous, due to their higher energy efficiency, to excel at swimming and diving than be subpar at both swimming and flying.

Penguins are also physiologically incapable of flying due to their reduced wingspan, large wing bones, large body mass and slow wing-beat frequency. These characteristics, however, provide penguins with the endurance and reduced drag to reach food sources at higher depths in the water. The adaptive evolution of a population to suit the environment can be seen in the various organisms that inhabit the planet. It is this natural selection and adaptive evolution that shapes the life around us.

To learn more about the flightlessness of penguins, see the interview with Bronx Zoo penguin expert, Nancy Gonzalez below.


To read more:

Elliott, K. H., Ricklefs, R. E., Gaston, A. J., Hatch, S. A., Speakman, J. R., & Davoren, G. K. (2013). High flight costs, but low dive costs, in auks support the biomechanical hypothesis for flightlessness in penguins. Proceedings of the National Academy of Sciences Proc Natl Acad Sci USA, 110(23), 9380-9384.
Olson-Manning, C. F., Wagner, M. R., & Mitchell-Olds, T. (2012). Adaptive evolution: Evaluating empirical support for theoretical predictions. Nat Rev Genet Nature Reviews Genetics, 13(12), 867-877.
Li, C., Zhang, Y., Li, J., Kong, L., Hu, H., Pan, H., . . . Zhang, G. (2014). Two Antarctic penguin genomes reveal insights into their evolutionary history and molecular changes related to the Antarctic environment.GigaScience Giga Sci, 3(1), 27. doi:10.1186/2047-217x-3-27
McNab, B. K.(1994). Energy Conservation and the Evolution of Flightlessness in Birds. The American Naturalist, 144(4), 628–642.
Wang, Xia, and Julia A. Clarke. “Phylogeny and Forelimb Disparity in Waterbirds.” Evolution 68.10 (2014): 2847-860. Academic Search Alumni Edition. Web. 13 Nov. 2015.
Hui, Clifford A. “Maneuverability of the Humboldt Penguin ( Spheniscus Humboldti ) during Swimming.” Can. J. Zool. Canadian Journal of Zoology 63.9 (1985): 2165-167. Web.

Systematic Penguin Evolution

Contributed by: Oceana Hopkins, Arooj Khalid, Kevin Lu

The core idea of modern evolutionary theory is that all life is descended from a common ancestor. Though the theory garners much scrutiny and skepticism, it can be explained in part through the simple mechanism of natural selection. Natural selection takes advantage of the variability that exists within the genome. Random mutations that occur in the genome are behind these variations and sometimes change the fitness of an organism. Natural selection dictates that those with higher fitness survive and reproduce; thus, certain traits are selected for within the species. This process explains how gradual change occurs and how complex organisms arise from simplistic ancestors. A common misconception regarding evolution is that life evolved randomly, or by chance. This misconception could arise because of the random nature of mutations that promote variability. Though randomness is an important component to evolutionary theory, natural selection and survival of those who are more biologically fit make sure that the process is non-random.

Known for their characteristic black and white “tuxedos”, penguins are an aquatic, flightless bird found in both warm and cold climates. Because such a large part of their lives are spent in the water, certain species of penguins will only exit the water to shed their feathers or to mate. Spending nearly 75% of their lives in the water foraging for food, penguins have developed very specific traits optimized for swimming.  Utilizing their strong forelimbs to propel their large bodies through the water, penguins have undergone very specific evolutionary changes that allow this mechanism to run smoothly. As discussed in Michael Habib’s paper on structural evolution, the strength of the bones in the forelimbs are significantly greater than that of birds who do not exhibit aqua-flying behavior (2009). In conjunction with increased bone density, more muscle mass also developed and aided in keeping the penguins warm in their cold feeding environment.

Closer inspection of the features that aid water-feeding behavior provides more evidence that disputes the misconception that evolution is random. As seen in 2006 by Slack and colleagues, macroevolution within penguins based on their fossils and mitochondrial genes was tracked and recorded. The evidence showed that the penguins’ bodies gradually adapted to the cold feeding environment over many generations. Additionally, researchers Thomas and colleagues observed in 2010 that cold water penguins have a flow of heat along their wings that originates from the brachial artery called the humeral plexus.  This vascular countercurrent heat exchanger (CCHE) provides penguins the opportunity to forage in cold water by limiting heat loss through the flippers. Scientists identified this adaptation through fossil evidence and, upon further research, learned it evolved after penguins lost the ability of aerial flight. Researchers have proposed the CCHE evolved to help balance the energy costs of longer foraging times, since the oceans were significantly cooler than penguin body temperature. Ultimately, researchers have concluded that the humeral plexus was instrumental in allowing penguins to be water feeders in subaquatic environments.


To learn more:

Clarke, J. A., D. T. Ksepka, R. Salas-Gismondi, A. J. Altamirano, M. D. Shawkey, L. D’alba, J. Vinther, T. J. Devries, and P. Baby. “Fossil Evidence for Evolution of the Shape and Color of Penguin Feathers.”Science 330 (2010): 954-57. Print

Fordyce, R. E. and Jones, C. M. 1990. The history of penguins, and new fossil penguin material from New Zealand. Pages 419-446 in Davis, L. S. and Darby, J. D. (editors), Penguin biology. Academic Press, San Diego. 467 p.

Habib, Michael. “The Structural Mechanics And Evolution Of Aquaflying Birds.” Biological Journal of the Linnean Society 99 (2009): 687-98. Print.

Stack, Kerryn E., Craig M. Jones, Tatsuro Ando, G. L. Harrison, R. Ewan Fordyce, Ulfur Arnason, and David Penny. “Molecular Biology and Evolution.” Early Penguin Fossils, Plus Mitochondrial Genomes, Calibrate Avian Evolution. Oxford Journals, Mar. 2006. Web. 13 Nov. 2015.

Subramanian S, Beans-Pico´n G, Swaminathan SK, Millar CD, Lambert DM. 2013 Evidence for a recent origin of penguins. Biol Lett 9: 20130748.

Thomas, D. B., D. T. Ksepka, and R. E. Fordyce. “Penguin Heat-retention Structures Evolved in a Greenhouse Earth.” Biology Letters 7 (2010): 461-64. Print.

Cancer: Evolutionary Fact or Fiction?

Contributed by Nicholas Eyrich, Jordan Feltes, Eric Ni, Somnath Das, Noah Steigelfest, and Evan Dackowski.

Cancer Heredity

Misconception: It is commonly perceived that cancer is hereditary, and one can either not have cancer in their family, thinking they are fine or have family members diagnosed and think it is a matter of time before they contract the disease.

Truth: Both of these notions grossly overlook the fact that most cancers are sporadic, meaning their onset is not due to family history, but rather due to gen1etic mutations and environmental exposures during one’s lifetime. Cancer is not heritable, but a predisposition to the disease can be (Peltomaki, 2012). For example, in our DNA we have two copies of each tumor suppressor gene, one from each parent. These genes keep cells from growing uncontrollably. So to lose function, one has to have mutations in both copies. Unfortunately, one can be born with a mutation in one copy, such as in Retinoblastoma (Rb). This means the gene is still expressed using the normal copy, but this confers a 50% increased predisposition for the disease bringing cells halfway closer to being cancer cells (Price et al., 2014).

Evolutionary Cancer Mutations

Misconception: It takes one bad mutation in one cell to get cancer, and cancer is one disease with all of cells in a tumor being equal.

Truth: Population biology is used to describe tumor growth and spread (metastasis), rather than arising from a single “bad” cell. Actually, it takes on average six to seven cumulative mutations (less in pediatric cancers) to confer disease, each one having been selected for during the previous cell generation. When mutations happen and build upon each other, the combination of changes can lead to cancer. (Yamamoto, Nakamura, & Haeno, 2015). Illustrated below. This supports cancer mostly being a disease of old age, as mutations take time to accumulate. Cancer essentially consists of many diseases that continue to harass the brains of researchers. Essentially, doctors have been able to treat for certain mutations, but once one important mutation is treated, another one can take over to drive relapse (Landau et al., 2015). Also, in tumors there ar2e different environments around cells fostering different mutations in various areas of the same tumor (Hardiman et al., 2015). Cancer is adapting to therapies that target mutations, making it so difficult to control.

DNA Damage

Misconception: DNA damage is rare, and we have little protection against it. Most cancer-causing agents (carcinogens) are processed chemicals not naturally found in nature.

Truth: DNA damage happens many times per day and our bodies have also evolved repair mechanisms in response to the need to correct such damage. In addition, the vast majority of cancer causin3g agents are naturally occurring substances we encounter on a daily basis (Bauer, Corbett, & Doetsch, 2015). The human body has evolved ways to counteract DNA-damaging events, for example during sunlight exposure, using molecular machinery and likewise other naturally occurring compounds (Nishisgori, 2015).



Bauer, Nicholas C., Anita H. Corbett, and Paul W. Doetsch. “The Current State of Eukaryotic DNA Base Damage and Repair.” Nucleic Acids Res Nucleic Acids Research (2015): n. pag. Web.

Hardiman, Karin M., Peter J. Ulintz, Rork D. Kuick, Daniel H. Hovelson, Christopher M. Gates, Ashwini Bhasi, Ana Rodrigues Grant, Jianhua Liu, Andi K. Cani, Joel K. Greenson, Scott A. Tomlins, and Eric R. Fearon. “Intra-tumor Genetic Heterogeneity in Rectal Cancer.” Lab Invest Laboratory Investigation (2015): n. pag. Web.

Landau, Dan A., Eugen Tausch, Amaro N. Taylor-Weiner, Chip Stewart, Johannes G. Reiter, Jasmin Bahlo, Sandra Kluth, Ivana Bozic, Mike Lawrence, Sebastian Böttcher, Scott L. Carter, Kristian Cibulskis, Daniel Mertens, Carrie L. Sougnez, Mara Rosenberg, Julian M. Hess, Jennifer Edelmann, Sabrina Kless, Michael Kneba, Matthias Ritgen, Anna Fink, Kirsten Fischer, Stacey Gabriel, Eric S. Lander, Martin A. Nowak, Hartmut Döhner, Michael Hallek, Donna Neuberg, Gad Getz, Stephan Stilgenbauer, and Catherine J. Wu. “Mutations Driving CLL and Their Evolution in Progression and Relapse.” Nature 526.7574 (2015): 525-30. Web.

Nishisgori, Chikako. “Current Concept of Photocarcinogenesis.” Photochem. Photobiol. Sci. 14.9 (2015): 1713-721. Web.

Peltomäki, Päivi. “Mutations and Epimutations in the Origin of Cancer.” Experimental Cell Research 318.4 (2012): 299-310. Web.

Price, E. A., K. Price, K. Kolkiewicz, S. Hack, M. A. Reddy, J. L. Hungerford, J. E. Kingston, and Z. Onadim. “Spectrum of RB1 Mutations Identified in 403 Retinoblastoma Patients.” Journal of Medical Genetics 51.3 (2013): 208-14. Web.

Weinberg, Robert A. The Biology of Cancer. New York: Garland Science, 2007. Print.

Yamamoto, Kimiyo N., Akira Nakamura, and Hiroshi Haeno. “The Evolution of Tumor Metastasis during Clonal Expansion with Alterations in Metastasis Driver Genes.” Sci. Rep. Scientific Reports5 (2015): 15886. Web.


Evolution of Methicillin-Resistant Staphylococcus Aureus

Contributed by Priya Chopra, Shoeb Lallani, Rahul Mohan, Vivek Sawhney, Matt Wu, Manal Zafar

Perhaps you may think that humans cannot influence the evolution of MRSA. However, this is not the case. For years, humans have used antibiotics to treat many types of bacterial infections, ranging from Staphylococcus aureus infection to Streptococcus. Antibiotics can be found in places you might not expect, such as hand soaps, cleaners, toothpaste, and in livestock that have contact with humans (Nerby et al., 2011). The use of antibiotics in a wide variety of places promotes the development of a diverse range antibiotic resistance in S.aureus.

A Video on The Evolution of MRSA

You may also think that MRSA evolved/continues to evolve randomly by chance. However, the fact that humans continually introduce numerous antibiotics to bacteria promotes the evolution of bacteria in a way that promotes its own survival. Humans provide the selective pressure to prompt bacteria to evolve characteristics that will maximize its fitness in its host. For example, if we introduce an antibiotic to a population, there may be a select few bacteria that have a mutation or gene that confers antibiotic resistance, which can then be passed onto future generations (vertical gene transfer). This leads to antibiotic resistance, and, to make things worse, resistance can then also be transferred by horizontal gene transfer (between different species) (Giedraitiene et al., 2011). For example, S. aureus can develop resistance to an antibiotic used to treat a nearby different bacterial infection, like tuberculosis, by means of horizontal gene transfer. This resistance can then be shared to the rest of the S. aureus population via vertical gene transfer.

Eventually, many strains of MRSA evolve, and new antibiotics need to be created in order to treat the strains. So, next time your doctor gives you antibiotics, think about the evolutionary consequences of introducing these antibiotics to your body.

To learn more…

Cogen A. L., Nizet V., Gallo R. L. (2009). Skin microbiota: a source of disease or defense? British Journal of Dermatology, 158(3): 442-455.

Fomda B. A., Thokar M. A., Ray P. (2014). Prevalence and genotypic relatedness of methicillin resistant Staphylococcus aureus in a tertiary care hospital. Journal of Postgraduate Medicine, 60(4): 386-9.

Giedraitiene A., Vitkauskiene A., Naginiene R., Pavilonis A. (2011). Antibiotic Resistance Mechanisms of Clinically Important Bacteria. Medicina, 47(3): 137-46.

McNulty C., Boyle P., Davey P. (2007). The public’s attitudes to and compliance with antibiotics. Journal of Antimicrobial Chemotherapy, 60: 63-68.

Micek S. T. (2007). Alternatives to Vancomycin for the Treatment of Methicillin-Resistant Staphylococcus aureus Infections. Clinical Infectious Diseases, 45: 184-190.

Nerby J.M., Gorwitz R., Harriman K. (2011). Risk factors for household transmission of community-associated methicillin-resistant Staphylococcus aureus. Pediatric Infectious Disease Journal, 30(11): 927-32.

Planet P. J., LaRussa S. J., Dana A., Smith H., Xu A. (2013). Emergence of the Epidemic Methicillin-Resistant Staphylococcus aureus Strain USA300 Coincides with Horizontal Transfer of the Arginine Catabolic Mobile Element and speG-mediated Adaptations for Survival on Skin. American Society for Microbiology, 4, 13.

Poole K. (2007) Efflux pumps as antimicrobial resistance mechanisms. Annals of Internal Medicine, 39(3): 162-76.

Wielders C. L., Fluit A., Schmitz F., mecA Gene Is Widely Disseminated in Staphylococcus aureus Population, Journal of Clinical Microbiology, 40(11): 3970-3975.  

Why You Should Thank Your Food Allergies

Contributed by Jimmy Shah, Sanjana Rao, and Laura Galarza


Did you know that over 15 million Americans suffer from food allergies today? Consider this. Every 3 minutes, a food allergy reaction sends someone to the ER. Given these severe, potentially life-threatening medical conditions that have no known cure, we think studying the origins of food allergies can have significant clinical implications. So what exactly is a food allergy?

Food allergies manifest as adverse immune system reactions to harmless food substances. Once the allergen enters the body, it will be recognized by and bind to serum immunoglobulin E (IgE) – antibodies found in the lungs, skin, and mucosal membranes. IgE is attached by FcɛRI surface receptors on mast cells, an immune cell that helps the body create inflammatory responses. Interestingly, studies have shown that the high-affinity IgE-FcɛRI receptor binding is involved in responding to not only allergen exposure, but also parasite invasion.

Symptom severity is correlated with IgE antibody concentration

Symptom severity is correlated with IgE antibody concentration

After the binding occurs, the allergen will cause antibody cross-linking on the mast cell surface and lead to something called mast cell degranulation, which means the mast cell will release its internal pro-inflammatory molecules, like histamines, leukotrienes, and prostaglandins, into the bloodstream. This will cause the onset of the allergy symptoms many of us may know well (especially in the pollen-rich spring) – sneezing, itching, coughing, hives, GI discomfort, etc. The most severe of these is anaphylaxis, a rapid and potentially life-threatening body state where blood pressure is lowered and emergency symptoms arise as a result. This brings us to our central question: why would evolution naturally select for us to be allergic to food that sustains us? The anomaly of food allergies and their past, present, and future benefits remain largely poorly-defined. However, research shows us that IgE antibody recognition of the allergen and shared defense mechanisms play a significant role in evolving allergic responses over time.


Although not fully understood, allergic responses are thought to have evolved from an immune defense mechanism against parasite invasion and other harmful toxin colonization. For years, scientists saw allergies as genetic accidents where aberrant IgE antibody production was just a mishap. But given the conservative nature of evolution, the IgE antibody class couldn’t have just arisen to be destructive only in the case of genetic disorders. Even if they did, evolution wouldn’t keep them around if they were solely harmful. In 1991, Margie Profet created the toxin hypothesis – the idea that responding to toxins and allergic reactions occur in very similar ways, that allergies are inherently toxic or affiliated with toxic substances, and that allergic responses mostly involve symptoms by which toxins are expelled (sneezing, vomiting, coughing, etc.) Last month, scientists at Stanford published evidence supporting the sustained positive evolutionary pressure to keep these IgE antibodies around. First, they found that in normal mice, previous exposure to venom allowed for greater survivability following a lethal venom injection, as compared to mice who were only treated with control solution. Then, they tested the role of the allergic pathway. Specifically, they studied three different types of mice responding to bee venom injections – mice without IgE, mice without IgE receptors on mast cells, and mice without mast cells at all. Unlike the normal mice, the three mutants did not benefit from previous venom exposure, since they did not have the key immunological players coordinating allergic response (Tsai, 2015). Although allergies have become less threatening in our daily lives, this allergic-type, IgE-associated immune response provides support for the idea that allergic responses are closely linked to the ways in which our bodies fight off toxins, long ago and today.

In another study published in October 2015, researchers at the London School of Hygiene & Tropical Medicine hypothesized that there must be some molecular similarity between parasites and allergen proteins, as the same branch of the immune system is found to kick in in both circumstances. After extensive data analysis, the team found that 2,445 known parasite proteins were structurally and sequentially (think base pairs A, C, T, G) similar to those found in the portion of the allergen that is prone to immune system attack. Further, measuring human cell immune response to a protein from a parasitic worm that was similar to a protein from a prevalent pollen allergen family revealed that blood serum reacted against both worm infection and the allergen via the same antibody mechanism (Tyagi, 2015).


Overall, the precise origin of food allergies has yet to be defined. However, we can infer that thousands of years ago, our ancestors may have consumed foods that contained harmful proteins or mimicked harmful substances, so allergies may have very well evolved to protect us. For example, someone could have ingested a raw plant that looked like a poisonous plant in the same family, so his body was on high alert. The IgE response naturally kicked in and perhaps was sustained throughout several generations as a heritable characteristic because it gave certain individuals an advantage over others in surviving and reproducing. As a result, those advantaged individuals likely passed on these beneficial traits, so eventually the proportion of individuals with these advantageous characteristics increased because those who didn’t, would lesser survivability.

This beneficial defense mechanism is not a novel idea – if unwanted substances enter the body, whether it just appears to be harmful or actually is, the organism’s ability to survive is potentially at stake. Thus, evolution would select for mechanisms by which these substances can be fought internally and expelled from the body. It therefore makes perfect sense that evolution would select for allergic responses as a means to protect one against destructive parasites and toxins.

Ultimately, food allergies account for $25 billion dollars in health costs each year, and cause 30,000 cases of anaphylaxis, 2,000 hospitalizations, and approximately 150 deaths annually. This significant burden on our population’s health warrants study of how allergic responses occur and the reasoning behind why they do. In doing so, perhaps we can find a cure! But for now, keep in mind that food allergies aren’t necessarily all bad and that they might actually be shielding you from something far worse.


Brandtzaeg, Per. 2010. Food Allergy: Separating the Science from the Mythology. Nature Reviews Gastroenterology & Hepatology 7, no. 7: 380–400.

Fitzsimmons, Colin Matthew, Franco Harald Fakone, and David William Dunne. 2014. Helminth Allergens, Parasite-Specific IgE, and Its Protective Role in Human Immunity. Frontiers in Immunology 5: 61.

Gross, Michael. 2015. Why did evolution give us allergies? Current Biology, no. 2: 53-55.

Liu, Andrew H. 2015. Revisiting the Hygiene Hypothesis for Allergy and Asthma. Journal of Allergy and Clinical ImmMatricardi, P. M. 2014. Molecular Evolution of the Allergy. Allergologie 37, no. 10: 423–24.

Machado, D. C., Horton, D., Harrop, R., Peachell, P. T. and Helm, B. A. (1996), Potential allergens stimulate the release of mediators of the allergic response from cells of mast cell lineage in the absence of sensitization with antigen-specific IgE. Eur. J. Immunol., 26: 2972–2980. doi: 10.1002/eji.1830261224

Platts-Mills, Thomas A. E. 2012. Allergy in Evolution. New Trends in Allergy and Atopic Eczema, edited by J. Ring, U. Darsow, and H. Behrendt, 96:1–6.

Ratnaparkhe, Milind B., Tae-Ho Lee, Xu Tan, Xiyin Wang, Jingping Li, Changsoo Kim, Lisa K. Rainville, et al. 2014. Comparative and Evolutionary Analysis of Major Peanut Allergen Gene Families. Genome Biology and Evolution 6, no. 9: 2468–88.

Sicherer, Scott H., and Hugh A. Sampson. 2009. Food Allergy: Recent Advances in Pathophysiology and Treatment. Annual Review of Medicine 60, no. 1 (2009): 261–77.

Tsai, Mindy, Phillip Starkl, Thomas Marichal. 2015. Testing the “toxin hypothesis of allergy: mast cells, IgE, and innate and acquired immune responses to venoms. Elsevier. Vol. 36: 80-87.

Tyagi, Nidhi, Edward Franell, Colin Fitzsimmons, Stephanie Ryan. Comparisons of Allergic and Metazoan Parasite Proteins: Allergy of the Price of Immunity. PLOS Computational Biology.

Wang, Jing, Litao Yang, Xiaoxiang Zhao, Jing Li, and Dabing Zhang. 2014. Characterization and Phylogenetic Analysis of Allergenic Tryp_alpha_amyl Protein Family in Plants Journal of Agricultural and Food Chemistry 62, no. 1: 270–78.

Zusi, Karen. 2015. An Evolutionary Basis for Allergies. The Scientist.

The Lilliput Effect: Trends in Body Size Following Ancient Mass Extinctions

Contributed by Ziqi Wu, Tian Mi, Lei Huang, Zhuo Li.

Imagine myriad fishes, including creatures the size of school buses, swimming in the Earth’s seas. Yup. That’s how things used to be 360 million years ago. It was not until the appearance of Devonian-Mississippian vertebrates that the modern range of body sizes became readily visible in the marine system. What happened in between these times? What made the creatures’ sizes shrink and spoiled the fun of scuba diving nowadays?

The answer is that a massive extinction happened about 359 million years ago, at the end of the Devonian Period. The scientists named it the Lilliput Effect: a temporary size reduction following mass extinction, which is usually temporary, but sometimes becomes persistent in specialized groups, such as birds, plankton, or island faunas. But how can a smaller size increase an organism’s fitness? One popular misconception is that the fittest organisms in a population are those that are strongest and largest. However, the Lilliput Effect has proved this wrong.


A giant fish has the length of a school bus before the die-off. However, after the asteroid hit earth and a mass extinction took place, the surviving fishes, and their descendants, are smaller since smaller size gives them an advantage.

The mechanism underlying the effect is controversial. One hypothesized model points to the effect of weather. Researchers (Dahl et al.) tracked down redox history of the atmosphere and oceans and found out that the radiation of large predatory fish (animals with high oxygen demand) correlates with atmosphere oxygenation. Therefore, a lower level of oxygen in the atmosphere might have played a role in the overall shrinkage. A temperature model based on Bergmann’s rule proposes that size is negatively influenced by temperature (Bergmann 1847). Previous studies suggested that warm-blooded vertebrate species are larger in colder climates than their congeners inhabiting warmer climates (Harries and Knorr 2009).

However, a more recent study points to another advantage of smaller size: smaller individuals grow and reproduce faster, and they adapt to their environments more quickly because of their relatively short generation times (Sallan and Galimberti 2015). Using holocephalans and ray-finned fishes as examples, they demonstrated that smaller vertebrates tend to have high reproductive rates, short generation times, and large populations. These traits may increase survival while promoting diversification via higher variation and population fragmentation.

Altogether, although there is empirical evidence suggesting that Lilliput effect could be a general response to environmental stress following various mass extinction events, there remain many puzzles to be solved.

For further reading, see:

Adam K. Huttenlocker and Jennifer Botha-Brink. 2013. Body size and growth patterns in the therocephalian Moschorhinus kitchingi (Therapsida: Eutheriodontia) before and after the end-Permian extinction in South Africa. Paleobiology 39(2), 353-277.

Bing Huang, David A.T. Harper, Renbin Zhan, Jiayu Rong. 2010. Can the Lilliput Effect be detected in the brachiopod faunas of South China following the terminal Ordovician mass extinction? Palaeogeography, Palaeoclimatology, Palaeoecology, Volume 285, Issues 3–4, Pages 277-286.

Keller, G., Abramovich,S. 2009. Lilliput effect in late Maastrichtian planktic foraminifera: Response to environmental stress. Palaeogeography, Palaeoclimatology, Palaeoecology 284: 47-62

Peter J. Harries, Paul O. Knorr. 2009. What does the ‘Lilliput Effect’ mean? Palaeogeography, Palaeoclimatology, Palaeoecology, Volume 284, Issues 1–2, Pages 4-10.

Richard J. Twitchett. 2007. The Lilliput effect in the aftermath of the end-Permian extinction event, Palaeogeography, Palaeoclimatology, Palaeoecology, Volume 252, Issues 1–2, Pages 132-144, ISSN 0031-0182.

Sallan L, Galimberti AK. 2015. Body-size reduction in vertebrates following the end-Devonian mass extinction.Science 350(6262):812-815.