By: Linda Huang, Shivani Seth, Shawn Kripalani, Anasua Bandyopadhyay and Nikita Maddineni
Imagine you’re living in the middle ages welding steel swords, leading your mundane life. Suddenly, your child is overcome with a horrid fever. Distraught, you also start to notice your child developing shockingly large lumps all over his body. What is going on? Soon, you learn that this nightmare is not only endangering your son’s life, but also the communities around you. Two weeks later, everyone around you has passed away, but for some reason you managed to survive. Why?
This so-called curse was actually known as the Black Plague that spread throughout Europe. The black death killed 75 to 200 million people and it peaked in Europe between the years of 1346 and 1353. It began with a rat infected with the bacterium Yersinia pestis. The bacteria infect humans by attacking the lymph nodes. They then begin to rapidly replicate, causing the lymph nodes to swell and become buboes. These buboes cause the immune system to go into septic shock, which is multiple-organ failure. This was one of the darkest points of European history, as 30-60% of Europe’s total population was killed. The methods of treatment ranged from visiting witch doctors to bathing in urine to turning to the church. Communities even started to live in the sewage systems after they became aware that it could be airborne. However, there was a small percentage of the population that was able to survive the plague. In the population that survived, researchers found that there was a mutation in the gene for the CCR5 cell membrane receptor called CCR5-∆32.
This is an example of natural selection, where the bubonic plague acted as the selection pressure for individuals with the mutation. These individuals with the delta-32 mutation had a higher fitness because they were able to survive and reproduce better compared to individuals who were susceptible to the black plague.
Figure 1: Top map shows regions of Europe during the black plague where the CCR5-∆32 mutation was present vs. regions where it was not present. Bottom map shows regions of Europe that were affected by the Black Plague vs regions that were not.
Coincidentally, research has shown that this mutation can also provide protection against HIV infection. In order for HIV to enter cells, the CCR5 receptor must be present on the surface of the cell. However, in individuals with the CCR5-∆32 mutation, the CCR5 receptor is not present on the cell membrane. Due to this mutation, individuals are resistant to HIV. This relationship between HIV and the CCR5-∆32 mutation is a way to debunk the misconception that all mutations are detrimental. In this case, having the mutation leads to increased fitness.
The protective effects of the CCR5 delta32 mutation against HIV infection are also being investigated as a potential long-term treatment option. Currently, antiretroviral therapy (ART) is the most widely used treatment for HIV, consisting of a combination of drugs that suppress progression of the disease and for reduce rates of transmission. However, ART is not a cure and individuals must rely on daily drug regimens for the entirety of their lives. Furthermore, the virus can eventually develop resistance to ART, leading to a need for more long-term treatment options.
In 2009, Hutter and other researchers identified an innovative approach using stem-cell transplantation. In a case study, a patient had HIV infection for ten years and acute myeloid leukemia. Researchers performed a stem-cell transplantation from bone marrow from an immune-compatible donor whose cells lacked expression of CCR5. The donor, who was homozygous for the CCR5 delta32 mutation, was resistant to the HIV infection. Researchers hoped that transplanting these cells with the mutation to the HIV-infected patient would confer resistance. After two transplantations, there was no recurrence of leukemia or detectable HIV in the bloodstream. The CD4+ T-cells in this patient have returned to the normal range and all carry the donor’s CCR5 gene. This patient has remained without any evidence of HIV infection for more than 8 years after discontinuation of ART, providing encouragement for stem cell transplantation as a more long-term treatment for HIV.
Figure 2A: Normal cell that has the CCR5 receptor. HIV can enter and infect the cell.
Figure 2B: Mutated cell without the CCR5 receptor. HIV is not able to enter and infect the cell, thus making the individual immune to the virus.
To learn more:
Petz, L.D., et al. 2015. Progress toward curing HIV infection with hematopoietic cell transplantation. Stem Cells Cloning 8: 109-116.
Cohn, S.K., & Weaver, L.T. 2006. The Black Death and AIDS: CCR5-Δ32 in genetics and history. Q J Med 99: 497-503.
Allers, K., et al. 2011. Evidence for the cure of HIV infection by CCR5Δ32/Δ32 stem cell transplantation. Blood 117(10): 2791-99.
Galvani, A.P., & Slatkin, M. 2003. Evaluating plague and smallpox as historical selective pressures for the CCR5-Δ32 HIV-resistance allele. PNAS 100(25): 15276-79.
Shariff, Mohammed. “10 Crazy Cures for the Black Death- Listverse.” List verse. N.p., 21 Jan. 2013. Web. 06 Dec. 2015.
Libert, F., et al. 1998. The CCR5 mutation conferring protection against HIV-1 in Caucasian populations has a single and recent origin in Northeastern Europe. Human Molecular Genetics 7(3): 399-406.
Stumpf, M.P., & Wilkinson-Herbots, H.M. 2004. Allelic histories: positive selection on a HIV-resistance allele. Trends in Ecology and Evolution 19(4): 166-8.
Hutter, G., et al. 2009. Long-Term Control of HIV by CCR5 Delta32/Delta32 Stem-Cell Transplantation. New England Journal of Medicine 360: 692-698.
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.
Let’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-.
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.
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.
Humans have a considerably larger brain size than would be predicted for an animal our size, and this considerable brain size has helped shape the evolution of humanity. But how did this increase occur?
One idea about how our brains increased in size is the expensive tissue hypothesis. Our brain consumes 20% of our energy demands at rest, so it’s a very energetically expensive organ. In order to increase the size of the brain, the expensive tissue hypothesis suggests that our bodies had to divert energy from other systems—like the muscles or gut—to our brains. Our brains exclusively use glucose as its form of energy, and recent research from anthropologists at Duke University has found evidence in our genes for the expensive tissue hypothesis. They compared the amount of proteins that bring glucose into brain and muscle cells and found that humans demonstrated significantly more mutations for genes that increased the expression of glucose transporter proteins in the brain and had fewer mutations that increased the expression of the glucose transporters in the muscles. In contrast, chimpanzees had greater glucose transporter expression mutations in muscles but not in the brain when compared to humans. The differential expression of glucose transporters in humans and chimps means that chimps are much stronger than humans because more energy is going to their muscles than their brains. A recent study comparing the strength of chimps and macaques to the strength of university basketball players found that the apes could pull much more weight than humans. We (modern humans) last shared a common ancestor with chimps more than 7 million years ago, when the evolutionary line between modern chimps and modern humans split. After that, selection must have acted to shape the use of glucose, and thus muscular strength, differently in these two evolving lineages. Together, these two studies support the expensive tissue hypothesis, where humans directed more energy to their brain for enhanced cognitive abilities.
Diverting energy away from the muscles to the brain may be a method that allowed our ancestors’ brains to expand, but how exactly did evolution select for a big brain in the first place?
One major hypothesis is called the cultural intelligence hypothesis. This emphasizes the importance of sociality, communication and social learning in selecting for a larger brain. Social communication and learning may have been selected for because they allow for cooperative food gathering strategies such as group hunting and foraging. Communication also would have facilitated the development of tools. If you can learn to make an effective spear, which allows you to hunt larger prey and feed more people, then your offspring and kin would benefit, in terms of increased survival and reproduction. Your offspring would only have a higher fitness, however, if you can teach them how to make the spear and they can pass on that information to other generations. This passing on of information across generations is called culture and is similar to the transmittance of heritable alleles, thus we can talk about culture and biology as simultaneously shaping our evolution.
Our ability to run long distances coupled with our ability to make tools and pass on the information of how to make tools both increased our behavioral ability to hunt, giving us a fitness advantage. Our behaviors can then increase or decrease fitness, which would shape a population’s expressed phenotypes (both biological and cultural phenotypes) resulting in evolutionary changes. Those evolutionary changes influence our biology, which interacts with our culture to further shape behavior. Of course, all of this is going on in the context of the environment, which determines if a particular trait is going to increase you and your offspring’s chances of survival and reproduction.
Thus culture can augment the heritable transformation of alleles that increase the fitness of organisms. The development of culture and transmission of knowledge increasingly shaped our fitness and evolution. The simultaneous effect of biological and cultural selection forces shaped our evolution and lead to an increase in brain size in our ancestors and allowed the genus Homo to arise.
The interaction of culture (which facilitated learning and effective hunting) and biological changes (which diverted more energy to the brain) with behavior may have allowed for the size of our ancestors’ brains to increase, resulting in the nearly three pound organ that we see today. These are only a few hypotheses on how the brain expanded, and they are not mutually exclusive. They all may have played some aspect in the evolution of our present-day brains. However, the main point is that no one specific factor played a role in our brain expansion. Instead, a confluence of factors has shaped who we are today.
For more information, check out these sites!
“Bigger Brains: Complex Brains for a Complex World.” Smithsonian Institute 11/28/2015. Web.
Babbitt, Courtney C., et al. “Genomic Signatures of Diet-Related Shifts During Human Origins.” Proceedings of the Royal Society of London B: Biological Sciences (2010). Print.
Bozek, Katarzyna, et al. “Exceptional Evolutionary Divergence of Human Muscle and Brain Metabolomes Parallels Human Cognitive and Physical Uniqueness.” PLoS Biol 12.5 (2014): e1001871. Print.
Fedrigo, O., et al. “A Potential Role for Glucose Transporters in the Evolution of Human Brain Size.” Brain, Behavior and Evolution 78.4 (2011): 315-26. Print.
Reader, Simon M., Yfke Hager, and Kevin N. Laland. “The Evolution of Primate General and Cultural Intelligence.” Philosophical Transactions of the Royal Society of London B: Biological Sciences 366.1567 (2011): 1017-27. Print.
Roberts, Roland G. “Jocks Versus Geeks—the Downside of Genius?” PLoS Biol 12.5 (2014): e1001872. Print.
Somel, Mehmet, Xiling Liu, and Philipp Khaitovich. “Human Brain Evolution: Transcripts, Metabolites and Their Regulators.” Nat Rev Neurosci 14.2 (2013): 112-27. Print.
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
Contributed to by Caitlin Brennan, Paige Hogen, Eliot Littlefield, Lauren Taylor and Kathryn Trinka
Many species produce pheromones to communicate with other members of their species. Most people think of pheromones as chemicals used to attract potential mates. However, studies have shown that insects such as butterflies, moths, and other insects produce pheromones with the opposite effect following mating (Greenfield 1981).
How could a mechanism that reduces mating have evolved? One hypothesis describes how these pheromones could have been favored due to male competition. Female Heliconius butterflies naturally release these pheromones when they are not ready to mate, but males also transfer pheromones to females during mating. This causes the female to involuntarily release the pheromone, repelling other males when she would otherwise be receptive to mating (Estrada et al. 2011).
Similar to butterfly pheromones, if a guy with a lot of cologne hugs a girl, she will smell like his cologne for the rest of the day. From that point on, other guys throughout the day will be off put by her smell.
When a male green-veined white butterfly begins to court a female, she initially responds with a refusal gesture. If she is carrying repellent pheromones from another male, this posture causes her to release these pheromones. The courting male perceives her rejection more strongly than he would without the pheromones, and is less likely to continue courting her. By preventing other males from mating with the female, the first male gains a fitness advantage by ensuring that the female’s offspring are his (Andersson 2004).
Interestingly, individuals in the butterfly species Heliconius sara generally mate with only one partner, in the same way that some people eat lunch with only one person; while individuals in the species Heliconius cydno mate with many partners, just as some people might eat lunch with a huge group of people (Estrada et al. 2011). Males of the species H. sara generally have weaker pheromones because in their butterfly culture of having one single mate, there is not as much competition between males to find a mate. In contrast, males of the species H. cydno have strong pheromones, because in their butterfly culture, competition deterring other males from mating with “his girl” dramatically increases the odds that that female will produce his offspring and not somebody else’s.
For Further Reading:
Catalina Estrada, Stefan Schulz, Selma Yildizhan and Lawrence E. Gilbert. 2011. Sexual Selection Drives the Evolution of Antiaphrodisiac Pheromones in Butterflies. Evolution. Vol. 65. No. 10: pp. 2843-2854.
Johan Andersson, Anna-Karin Borg-Karlson and Christer Wiklund. 2004. Sexual Conflict and Anti-Aphrodisiac Titre in a Polyandrous Butterfly: Male Ejaculate Tailoring and Absence of Female Control. Proceedings: Biological Sciences. Vol. 271, No. 1550: pp. 1765-1770.
Ally R. Harari, Tirtza Zahavi and Denis Thiéry. 2011. Fitness Cost of Pheromone Production in Signaling Female Moths. Evolution. Vol. 65, No. 6: pp. 1572-1582
Michael D. Greenfield. Moth Sex Pheromones: An Evolutionary Perspective. 1981. The Florida Entomologist. Vol. 64, No. 1: pp. 4-17
Johan Andersson, Anna-Karin Borg-Karlson, Namphung Vongvanich, Christer Wiklund. 2007. Male sex pheromone release and female mate choice in a butterfly. Journal of Experimental Biology. 210: 964-970
Romina B. Barrozo, Christophe Gadenne, Sylvia Anton. 2010. Switching attraction to inhibition: mating-induced reversed role of sex pheromone in an insect. Journal of Experimental Biology. 213: 2933-2939
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.
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).
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:
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.
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. http://doi.org/10.1098/rsos.150196
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.
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.
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.
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.
Contributed by Ziad Jowhar, Elie Nwefo, Yasmine Alkhalid, Sai Greeshma Magam, Rasika Tangutoori, & Shray Ambe
Imagine waking up everyday with fatigue and joint pain. You constantly fear having a stroke or heart attack that could cause your premature death. Unfortunately, this is a reality for patients dealing with severe forms of sickle cell disease (SCD).
SCD is caused by a recessive mutation on chromosome eleven and primarily affects the cardiovascular system. Red blood cells are essential for transporting oxygen to the rest of your body. These cells are normally round, allowing them to fit through small blood vessels. Individuals with SCD, who are homozygous for the sickle cell allele, have red blood cells that are crest-shaped instead. This deformity can cause blood clots, ultimately leading to tissues in the body to become oxygen deprived. If this blockage occurs in a major vessel, it can cause a stroke, heart attack, or even death. However, there is hope for individuals with the disease, as recent research has found that SCD can be cured through bone marrow transplant. Sadly though, there are limitations — it has been more successful in younger patients who receive transplants from a full sibling or matched donor.
But how can such a harmful disease manage to survive? One misconception is that the fittest organisms in a population are the healthiest. Shouldn’t the sickle cell trait have been erased from the human population long ago since it lowers life expectancy?
Before we dive into why the sickle cell trait still exists, let’s take a step back and learn a little more about SCD’s effects and treatment options from Dr. Kirshma Khemani, a specialist in pediatric hematology and oncology:
Could you give a brief background on yourself and your current research?
What are the symptoms of sickle cell disease?
What are the current treatment options for sickle cell disease?
What are the risks of each treatment option for sickle cell disease?
Recently stem cell therapy has been identified as a potential cure for sickle cell disease, what are your views on these findings?
Now, let’s get back to the big question: how could this trait continue to prevail? The sickle cell trait has been found in regions of the world where malaria occurs: 10-40% of the population carries the sickle cell mutation. But wait a second. What is malaria and how is it related to SCD?
Malaria is a life threatening disease that is caused by a parasite and is transmitted through mosquito bites. There is a correlation between malaria and SCD: individuals who carry the sickle cell trait, who are heterozygous for the sickle cell allele, have a protective advantage against malaria. This occurs because the parasite that causes malaria cannot mature in the oxygen-deprived sickled red blood cells and dies.
Although SCD does have several disadvantages, the sickle cell trait has been able to survive in the population due to its protective role against malaria.
For additional information, see the following references:
Gemmell NJ, Slate J. 2006. Heterozygote advantage for fecundity. PLoS ONE 1(1).
Kwiatkowski, D. P. 2005. How malaria has affected the human genome and what human genetics can teach us about malaria. The American Journal of Human Genetics, 77(2), 171-192.
Larremore, D. B. et al. 2015. Ape parasite origins of human malaria virulence genes. Nature Communications Nat Comms, 6.
Saraf, S. L. et al. 2015. Nonmyeloablative stem cell transplantation with alemtuzumab/low-dose irradiation to cure and improve the quality of life of adults with sickle cell disease. Biology of Blood and Marrow Transplantation.
Sellis, D., Callahan, B. J., Petrov, D. A., & Messer, P. W. 2011. Heterozygote advantage as a natural consequence of adaptation in diploids. Proceedings of the National Academy of Sciences, 108(51), 20666-20671.
Williams, T. N. et al. 2005. An immune basis for malaria protection by the sickle cell trait. PLoS Med PLoS Medicine 2: 441-445.
Contributed by Esther Lee, Rina Lee, Jasmine Labarca, Heather Wang, Phoenix Phung, Enakshi Das
Did you ever wonder what our ancestors ate? I do! The Paleo diet, also known as the caveman diet, Stone Age diet, and hunter-gatherer diet, consists of foods that are assumed to have been available to our ancestors before the Agricultural Revolution began around 333 generations ago. Our ancestors mainly ate meat, fruits, and vegetables before agriculture was developed, but now the Western diet has expanded to include a high number of cereal-grains, milk products, sugar, sweeteners, separated fats and alcohols, which now make up around 70% of our diet (Cordain et al., 2005). These new food sources were made available by the Agricultural and Industrial Revolutions.
During prehistoric times, our ancestors ate raw, unprocessed foods, which require much more energy to digest. Nowadays, cooking, through the process of heating and pounding, breaks down the food, so food is not only easier, but also more efficient to digest (Gibbons 2015). This transition underlies the expensive tissue hypothesis (Suburu 2013), which links changes in diet to evolution of the human brain. The hypothesis is that the brain and gut tissue both require lots of energy, so as our brains became larger, the gut size became smaller. Cooking also allowed us to absorb more energy from food, further shrinking our gut, and allowing us to expand our brain.
Some people think that the Paleo diet is healthier because it is what sustained our ancestors and it is what we are thus adapted to eat. Instead of getting calories from processed foods, “Paleo dieters” get their nutrients through meat and raw, unprocessed foods. Many critics argue that the Paleo diet lacks food variety and believe that humans are adapted to consuming a varieties of foods, including those available in our modern diet.
This presentation explores the pros and cons of the two diets:
However, neither diet may be optimal for all individuals because of variation in the human population. Each individual reacts differently to the foods offered in each diet (Wan). For example, based on your genes, you can have a sweeter tooth than your friends (Gibbons 2015). There will always be environmental and cultural factors that will determine which diet is the best for you!
For more information see:
Ameur, Adam et al. “Genetic Adaptation of Fatty-Acid Metabolism: A Human-Specific Haplotype Increasing the Biosynthesis of Long-Chain Omega-3 and Omega-6 Fatty Acids.” American Journal of Human Genetics 90.5 (2012):809-820
Boers, Inge, Frits AJ Muskiet, Evert Berkelaar, Erik Schut, Ria Penders, Karine Hoenderdos, Harry J. Wichers, and Miek C. Jong. 2014. Favourable Effects of Consuming Palaeolithic-type Diet on Characteristics of the Metabolic Syndrome: A Randomized Controlled Pilot-study. Lipids in Health and Disease 13:160.
Burger, J., M. Kirchner, B. Bramanti, W. Haak, and M.G. Thomas. “Absence of the Lactase-persistence-associated Allele in Early Neolithic Europeans.” Absence of the Lactase-persistence-associated Allele in Early Neolithic Europeans. N.p., 27 Dec. 2006. Web. 30 Nov. 2015.
Cordain, L., Eaton S.B., Sebastian A., Mann N., Lindeberg S., Watkins B., O’Keefe J., Brand-Miller J. 2005. “Origins and Evolution of the Western diet: health implications for the 21st century. The American Journal of Clinical Nutrition 81: 341-354.
Eaton, S.B., Cordain, L. 1997. Evolutionary Aspects of Diet: Old Genes, New Fuels: Nutritional Changes Since Agriculture. World Rev Nutr Diet 81: 26-37.
Eaton, Stanley Boyd, and Stanley Boyd Eaton Iii. “Paleolithic vs. Modern Diets – Selected Pathophysiological Implications.” European Journal of Nutrition 39.2 (2000): 67-70.
Frassetto, L. A., M. Schloetter, M. Mietus-Synder, R. C. Morris, and A. Sebastian. 2009. Metabolic and Physiologic Improvements from Consuming a Paleolithic, Hunter-gatherer Type Diet. European Journal of Clinical Nutrition Eur J Clin Nutr 63: 947-55.
Gibbons, Ann. “The Evolution of Diet.” National Geographic. N.p., n.d. Web. 30 Nov. 2015.
Jew, Stephanie, Suhad S. AbuMweis, and Peter J.H. Jones. 2009. Evolution of the Human Diet: Linking Our Ancestral Diet to Modern Functional Foods as a Means of Chronic Disease Prevention. Journal of Medicinal Food.
Klonoff, David. “The Beneficial Effects of a Paleolithic Diet on Type 2 Diabetes and Other Risk Factors for Cardiovascular Disease.” Journal of Diabetes Science and Technology 3.6 (2009): 1229-232. Web.
Kowalski, L. M., and J. Bujko. “Evaluation of Biological and Clinical Potential of Paleolithic Diet.” Rocz Panstw Zakl Hig 63.1 (2012): 9-15. Pub Med. Web. 30 Nov. 2015.
Leonard, William R. “Food for Thought. Dietary Change Was a Driving Force in Human Evolution.” Scientific American (2003): n. pag. ResearchGate. Web. 30 Nov. 2015.
Martens, E., Lowe, E., Chiang, H., Pudlo, N., Wu M., McNulty N., Abbott, D., Henrissat, B., Gilbert, H., Bolam, D., Gordon, J. 2011. Recognition and Degradation of Plant Cell Wall Polysaccharides by Two Human Gut Symbionts. PLOS Biology 9.12.
Milton, Katharine. “The Critical Role Played by Animal Source Foods in Human (Homo) Evolution.” Journal of Nutrition 133:3893S-3897S.
O’dea, K. “Marked Improvement in Carbohydrate and Lipid Metabolism in Diabetic Australian Aborigines after Temporary Reversion to Traditional Lifestyle.” Diabetes 33.6 (1984): 596-603. PubMed. Web. 30 Nov. 2015.
Schaeffer, Juliann. “Evolutionary Eating — What We Can Learn From Our Primitive Past.” Today’s Dietitian 11.4 (2009): 36. Today’s Dietitian. Web. 30 Nov. 2015.
Simmons, A. L., J. J. Schlezinger, and B. E. Corkey. “What Are We Putting in Our Food That Is Making Us Fat? Food Additives, Contaminants, and Other Putative Contributors to Obesity.” Curr Obes Rep 3.2 (2014): 273-85. Print.
Suburu, Janel, Zhennan Gu, Haiqin Chen, Wei Chen, Wei Chen, Hao Zhang, and Young Q.Chen. Fatty Acid Metabolism: Implications For Diet, Genetic Variation, and Disease. Food Biosci (2013) 4: 1-12. .
Tarantino, G., Citro, V., Finelli, C. 2015.Hype or Reality: Should Patients with Metabolic Syndrome-related NAFLD Be on the Hunter-Gatherer (Paleo) Diet to Decrease Morbidity?. Journal of Gastrointestinal and Liver Diseases J Gastrointestin Liver Disease 24: 359-368.
Wan, Samantha. Evolution in the Processed Foods Industry: Exploring the Impact of the Health Foods Movement. N.p.: U of Southern California, n.d. Print.
Contributed by Aaron Karas, Yash Patel, and Kristin Larsen
Have you ever wondered about the evolution of man’s best friend? Scientists believe it began between 30,000 and 130,000 years ago when humans began to control wolves. Today, as a result of mutation and artificial selection, there are hundreds of different breeds of dogs. Considering there are currently 339 breeds of dogs recognized by the World Canine Organization, it is easy to forget that they all belong to the same species. This profusion of breeds today reflects intense and purposeful interbreeding of dogs over the past 150 years.
The dog, Canis familiaris is a direct descendent of the gray wolf, Canis lupus. Genetic evidence from an ancient wolf bone discovered lying on the tundra in Siberia’s Taimyr Peninsula revealed that wolves and dogs may have split from their common ancestor at least 27,000 years ago. This first divergence was followed by what is thought to be the second divergence uncovered by research done in 2014. Ultimately this indicates that wolf populations from which dogs originated have gone extinct, and that the current wolf diversity from each region represents new, younger wolf lineages.
Since diverging from the gray wolf, the dog has undergone thousands of years of evolution. It may seem implausible that humans could have significantly altered the course of this species’ evolution considering this long time span. However, the idea that humans cannot influence evolution because it occurs over such long periods of time is a common misconception. Evolution does not necessarily occur over millennia. In fact, in some experiments it has been shown to occur in just a matter of weeks. In the case of dogs, a significant portion of the diversity that we see today can largely be attributed to the artificial selection that has occurred over the past 150 years. Artificial selection is the process by which humans intentionally breed a species with the hope of producing offspring with a particular set of traits. And this is what we see with dog breeding. Continued selection for certain traits within dog lineages eventually leads to the generation of new breeds, each of which has a unique form and personality.
For example, the German Shepherd breed first appeared in Germany in the late 19th century. The first declared German Shepherd was the result of decades of breeding dogs for the purpose of herding and guarding sheep. Desired traits, such as intelligence and strength, were thus being selected for. After continued selection for traits desired in a herding and guard dog, the German Shepherd evolved to become the notably territorial, loyal and attentive breed that it is today.
If you’re interested in learning more about this topic, please refer to the following articles:
Larson, G., E. K. Karlsson, A. Perri, M. T. Webster, S. Y. W. Ho, J. Peters, P. W. Stahl, P. J. Piper, F. Lingaas, M. Fredholm, K. E. Comstock, J. F. Modiano, C. Schelling, A. I. Agoulnik, P. A. Leegwater, K. Dobney, J.-D. Vigne, C. Vila, L. Andersson, and K. Lindblad-Toh. “Rethinking Dog Domestication by Integrating Genetics, Archeology, and Biogeography.” Proceedings of the National Academy of Sciences 109.23 (2012): 8878-883.
Shannon, Laura M., Ryan H. Boyko, Marta Castelhano, Elizabeth Corey, Jessica J. Hayward, Corin Mclean, Michelle E. White, Mounir Abi Said, Baddley A. Anita, Nono Ikombe Bondjengo, Jorge Calero, Ana Galov, Marius Hedimbi, Bulu Imam, Rajashree Khalap, Douglas Lally, Andrew Masta, Kyle C. Oliveira, Lucía Pérez, Julia Randall, Nguyen Minh Tam, Francisco J. Trujillo-Cornejo, Carlos Valeriano, Nathan B. Sutter, Rory J. Todhunter, Carlos D. Bustamante, and Adam R. Boyko. “Genetic Structure in Village Dogs Reveals a Central Asian Domestication Origin.” Proceedings of the National Academy of Sciences Proc Natl Acad Sci USA (2015): 201516215.
Parker, H. G. “Genetic Structure of the Purebred Domestic Dog.” Science 304.5674 (2004): 1160-164.
Skoglund, P., A. Gotherstrom, and M. Jakobsson. “Estimation of Population Divergence Times from Non-Overlapping Genomic Sequences: Examples from Dogs and Wolves.” Molecular Biology and Evolution 28.4 (2010): 1505-517.
Vila, C. “Multiple and Ancient Origins of the Domestic Dog.” Science 276.5319 (1997): 1687-689.
Akey, J. M., A. L. Ruhe, D. T. Akey, A. K. Wong, C. F. Connelly, J. Madeoy, T. J. Nicholas, and M. W. Neff. “Tracking Footprints of Artificial Selection in the Dog Genome.” Proceedings of the National Academy of Sciences 107.3 (2010): 1160-165.
Contributed by: Maria Berce, Danny Kang, Travise Kinney, Fariah Majid, & Alex Zachowski
Have you ever wondered why certain diseases are maintained in the human population if they are a threat to human health? It turns out that in some situations, a particular trait, potentially even a disease, may help an individual survive and thus can be maintained in a population over time.
Most laypeople believe that mental health illnesses occur when an individual carries a trait that is detrimental to humans. However, in reality, a trait can become a disorder when something that allows an individual to thrive in one environment becomes an obstacle in a different environment. For example, think about our ancestors who were hunters and gatherers. In their environment, being hyper-aware of their surroundings was beneficial because it protected them from attacks by predators. But what if this hyper-awareness was passed down to their offspring and was maintained generation after generation? Now, in our modern environment, being hyper-aware while sitting at a desk for hours on end each day would not lead to “productive” behavior. Thus, the trait of being hyper-aware may now perceived as an illness, specifically Attention-Deficit Hyperactivity Disorder (ADHD).
This animation illustrates the misconception that unfavorable traits are always selected against.
Just because a trait is maintained in a population does not mean it is favored by natural selection. Take a look below and see if you can now understand the incidence and progression of mental health illnesses through an evolutionary lens.
Attention-Deficit Hyperactivity Disorder (ADHD). There have been a lot of articles in the media lately about the sharp rise in the number of children in the U.S. and other western nations who are being diagnosed with ADHD. The U.S. government’s Center for Disease Control, or CDC, found that over 11% of children between the ages of four and 17 were diagnosed with ADHD in 2011, and that the rates of diagnosis have been growing by an average of three percent each year from 1997 to 2006. There is some disagreement over whether some of this increase is due to an over-diagnosis of the condition; however, the fact remains that ADHD is widespread and increasing. According to the CDC, children must have six or more symptoms of inattention and six or more symptoms of hyperactivity and impulsivity in order to be classified as ADHD. It is easy to see how these symptoms could make any child’s life a lot more difficult.
But another way of looking at ADHD has recently gained a following in the scientific community. Rather than looking at ADHD as a disorder, researchers have begun to look at it from the perspective of human evolution. In an article published in Journal of the American Academy of Child and Adolescent Psychiatry in 1997, Jensen and others hypothesized that ADHD is “an adaptation that reflects the optimization of brain function to some environments at the cost of poorer response to the demands of other environments.” In plain English, these scientists hypothesize that some children are genetically programmed to behave in a manner that may be disruptive in an academic or social setting.
Thomas Hartmann, a popular author and radio talk show host, wrote an entire book on this subject, titled “The Edison Gene: ADHD and the Gift of the Hunter Child.” In this book, Hartmann points out that Thomas Edison was expelled from school in the third grade for behavior that today would be labeled as symptomatic of ADHD. In his book, Hartmann argues that individuals with ADHD possess traits that were useful to humans during hunter-gatherer times and now individuals with these same traits are hardwired to be successful innovators, entrepreneurs, explorers, and inventors. Hartmann insists that these people shouldn’t be seen as “disordered” but as vital to our society and its progress, and calls for new alternative education methods for children with ADHD.
Interestingly, what was at once useful in protecting oneself from predators may now be valuable in a crime-infested neighborhood, for example. These scientists see hyper vigilance of one’s surroundings, hyperactivity that leads to an in-depth exploration of those surroundings, and fast response to stimuli – what others might label impulsivity – as “benefits” given the right environment.
Post-Traumatic Stress Disorder (PTSD). Post-traumatic stress disorder is a complex mental health condition that severely impacts the lives of those affected. Occurring after some sort of trauma, symptoms of PTSD include flashbacks, nightmares, and anxiety. According to PTSD United, a charity that provides support to sufferers, over 70% of adults in the United States will experience a trauma over the course of their lifetime, but only 1 in 5 of those people will go on to experience symptoms of PTSD. So why do some people get PTSD and not others?
In a 2004 article published in Clinical Psychology Review, psychologist and sociologist Michael Christopher argues that behaviors associated with PTSD, such as hyper-awareness, replaying the event in one’s head, and maintaining emotional distance from others, are hallmark “adaptive behaviors” to extreme threats. In other words, people who go through a traumatic situation such as war or robbery at gunpoint are psychologically and biologically transformed by the experience, resulting in the behaviors that we refer to as PTSD. These behaviors, Christopher argues, would all be beneficial to avoiding a similar future danger if they did not become pathological. Thus, in a sense, debilitating PTSD is essentially an “over-adaptation” by the human organism to the need to avoid severe dangers that may re-occur.
Anxiety Disorders. According to the National Institute of Mental Health, about 40 million adults are affected by an anxiety-related disorder, and rates have increased for the past 50 to 70 years. Why are mental disorders such as anxiety persisting in our population? Evolutionary biologists believe that anxiety, also referred to as the fight-or-flight response, was beneficial to our early ancestors when avoiding predators. This response increases heart rate and blood flow to muscles, and prompts us to respond faster in the face of danger. Today, many of us live in relatively peaceful environments, where our mean of survival is typing on a computer for eight hours a day. Although a certain amount of anxiety is beneficial in this environment as well, genetic predisposition to an anxiety disorder, which was selected for as a result of the environment of our ancestors, accounts for the fight-or-flight response even when we are not faced with grave danger.
We see that the behaviors that characterize these health conditions can be beneficial in some environments but not in others. An environment can determine the extent to which behaviors are harmful to the individual, based on the set of traits expressed by that individual. Although traits that characterize ADHD, PTSD, or anxiety disorders may have been beneficial in other environments, like previous societies, natural selection cannot remove these traits just because the modern environment may not value them. Since there is often no direct fitness consequence to having these mental illnesses , individuals who are diagnosed still pass on their genes, allowing for the illnesses to persist in a population.
When asking members of the Emory University community about their perceptions of mental health disorders, the responses we get are very interesting, some of which acknowledge the ways in which traits that characterize mental illnesses can be beneficial in today’s environment.
For further information, please refer to the following publications:
Avishai-Eliner, S., Brunson, K.L., Sandman, C.A., & T.Z. Baram. 2002. Stressed-out, or in (utero)?Trends Neurosci. 10: 518-24.
Byars, S.G. 2010. Natural Selection in a Contemporary Human Population. Proceedings of the National Academy of Sciences of the United States of America 107: 1787-792.
Christopher, M. A Broader View of Trauma: A biopsychosocial- evolutionary view of the role of traumatic stress response in the emergence of pathology and or growth. Clinical Psychology Review 24.1: 75-98.
Draganski, B., Gaser, C., Busch, V., Schuierer, G., Bogdahn, U., & A. May. 2004. Neuroplasticity: Changes in Grey Matter Induced by Training. Nature.
Hartmann, T. The Edison Gene. Vermont: Park Street Press, 2003. Print.
Gonçalves, V., Andreazza, A., & J. Kennedy. 2014. Mitochondrial Dysfunction in Schizophrenia: An Evolutionary Perspective. Springer-Verlag Berlin Heidelberg.
Jensen, P., Mrazek, D., Knapp, P., Steinberg, L., Pfeffer, C., Schowalter, J., Shapiro, T. 1997. Evolution and Revolution in Child Psychiatry: ADHD as a Disorder of Adaptation. Journal of the American Academy of Child and Adolescent Psychiatry 36.12: 1672-1681.
Lee, Y., Yamaguchi, Y., & Y. Goto. Neurodevelopmental Plasticity in Pre- and Postnatal Environmental Interactions: Implications for Psychiatric Disorders from an Evolutionary Perspective. Neural Plasticity.
Platter, B.E. 2009. Evidence of Contemporary Modern Human Evolution Contained Within the Human Genome. Lethbridge Undergraduate Research Journal.
Twenge, J. 2000. The Age of Anxiety? Birth Cohort Change in Anxiety and Neuroticism, 1952-1993. Journal of Personality and Social Psychology.
Twenge, J. 2008. Generational differences in psychological traits and their impact on the workplace. Journal of Managerial Psychology.
Twenge, J. 2012. Generational Differences in Young Adults’ Life Goals, Concern for Others, and Civic Orientation, 1966–2009. Journal of Personality and Social Psychology.
Weinstock, M. 2008. The long-term behavioural consequences of prenatal stress. Neuroscience and Biobehavioral Reviews 32: 1073–1086.
Centers for Disease Control and Prevention, 2015. Attention-Deficit/Hyperactivity Disorder (ADHD) Data and Statistics. Accessed December 1, 2015 (http://www.cdc.gov/ncbddd/adhd/data.html).
The Decline of Play and Rise in Children’s Mental Disorders. (n.d.). Retrieved from https://www.psychologytoday.com/blog/freedom-learn/201001/the-decline-play-and-rise-in-childrens-mental-disorders
Facts & Statistics | Anxiety and Depression Association of America, ADAA. (n.d.). Retrieved from http://www.adaa.org/about-adaa/press-room/facts-statistics
PTSD United, 2013. PTSD Statistics. Accessed December 1, 2015 (http://www.ptsdunited.org/ptsd-statistics-2/).