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Contributed by Ruthe Terfie Have you ever wondered where modern humans originated? Well, if you have, you’re not alone. Many scholars in the past, and even the present, have asked the same question and debated many hypotheses. The universally accepted … Continue reading
Contributed by Sarah Meadows
Climate change has the potential to shape evolutionary change in species, and has already done so in a few species around the planet. Climate change, or global warming as it is also called, can exact selectional pressure on species because of how it changes the habitat. Changing temperatures is perhaps the most well-known effect of climate change. Climate change can exert selectional pressure because not all species are fit enough to survive when their habitat changes.
One of the challenges with studying climate change and evolution is that it can be hard to distinguish between plastic responses and genetic changes. Plasticity is a species’ ability to adapt to changing conditions without their genetics, or their DNA, being changed. If a species breeding time is earlier than before and there is a correlation with warmer temperatures, for example, it could be because most individuals have the ability to begin breeding earlier (a plastic response), or it could be because individuals that happen to breed earlier have higher survival and reproduction, and they pass this early breeding trait onto their offspring. The latter scenario represents evolution by natural selection. Much of the research done so far on the subject has measured a change in life history traits but has not determined if the cause is a genetic change or phenotypic plasticity.
Species can respond to climate change in a few ways. They can change their life history traits, they can expand or shift their range, or they can go extinct. The latter has already happened to some amphibian populations, such as the golden toad and Monteverde harlequin frog in Costa Rica.
Some species that have been studied extensively on the subject are Drosophila flies, Darwin’s finches, and many other bird species. Some Drosophila have been found to exhibit genetic changes in the northern ranges that are very similar to ones from their southern ranges, suggesting that they either migrated northwards or there was directional selection for those genes. Some other changes that have been observed in other species due to climate change are ranges moving northwards, egg laying and breeding periods happening earlier, and migration happening later.
A few species of Drosophila have recently experienced genetic changes that have been attributed to climate change.
Even though some species have the ability to respond to climate change, such as adapting to the new conditions or moving, not all species can do so. Amphibians, for example, are hit very hard by it, with high rates of extinction compared to other vertebrates. Coral reefs are also hit hard by climate change because higher CO2 levels and bleaching (losing their microbial partners) is a problem. Another problem that is posed by climate change is that if two species have coevolved and are symbiotic with each other, one species could experience evolution due to climate change and the other may not. For example, a pollinating insect could emerge too early before the plant species it usually pollinates has bloomed.
Artic terns are one species of birds whose breeding date has advanced, possibly because of climate change. This is an example of a phenotypic change.
Insects can be affected by asynchrony, for example when a butterfly hatches earlier then its host plant.
Climate change presents a new, challenging influence on habitats, and its long term effects on species diversity and their evolution have yet to be determined, but in the short term it is clear that climate change does have an effect on the evolution of species.
For more information, see:
Balanyá, J., Oller, J. (2006) Global Genetic Change Tracks Global Climate Warming in Drosophila subobscura. Science. 313: 1773-1775.
Gienapp, P., Teplitsky, C., Alho, J. S., Mills, J. A. and Merila, J. (2008), Climate change and evolution: disentangling environmental and genetic responses. Molecular Ecology, 17: 167–178.
Grant, P., Grant, R. (1995), Predicting microevolutionary responses to directional selection on heritable variation . Evolution, 49: 241-251.
Levitan, M., Etges, W., (2005) Climate change and recent genetic flux in populations of Drosophila robusta. BMC Evolutionary Biology, 5:4
MØller, A. P., Flensted-Jensen, E. and Mardal, W. (2006), Rapidly advancing laying date in a seabird and the changing advantage of early reproduction. Journal of Animal Ecology, 75: 657–665.
Parmesan, C. (2006), Ecological and evolutionary responses to recent climate change. Annual Review of Ecology Evolution and Systematics, 37: 637-669.
Pounds, A., Bustamante, M. (2006), Widespread amphibian extinctions from epidemic disease driven by global warming. Nature, 439: 161-167
Contributed by So Heui Kim
This black and white photo was created by using the sandwich technique. I randomly chose the faces from a magazine. The third negative is a photo of human cells. My intention was to create a photo that illustrates how our cells and the genes within them are involved in our mate choice.
Despite a lot of interest, it is not clear what traits determine what mates humans choose. It sometimes seems that each individual has different preferences. Humans can be influenced by many factors, including parental guidance, the environment, education, attractiveness, and the media. Some research suggests that despite these influences, human mate choice is based on genetic similarity.
The major histocompatibility complex is believed to take a huge role in human immune system. The MHC molecules bind pathogen-derived peptide fragments and display them on the cell surface to be recognized by the T cells (Janeway, Travers, Walport et al, 2001). These MHC molecules help our body to recognize and eliminate the harmful pathogens. Therefore, maintaining MHC diversity is a key to human survival. The more diversity there are in MHC molecules, the more pathogens will be killed.
In “Major histocompatibility complex peptide ligands as olfactory cues in human body odor assessment”, researchers found out that humans have the ability to detect and evaluate body odor by MHC peptides. In the experiment, human volunteers were asked to apply two different solutions of MHC peptide ligands under their armpits. Then, the participants had to decide which armpit smell they preferred. Participants preferred their body odor more typical of individuals with an MHC profile like their own. This result strongly supports the findings that humans with similar MHC alleles also have similar perfume preference. Unlike when smelling armpits, women prefer the odor of shirts worn by men with different MHC alleles. By mating with a person who has dissimilar MHC genotype, they will maintain their offspring’s MHC diversity.
Wearing perfume is considered one way to attract a mate. Based on the results from the experiments above, we can consider how MHC should impact perfume selection. From the armpit experiment, we can predict that people will prefer to wear perfumes that are similar to their MHC peptides. In “Evidence for MHC-correlated perfume preferences in humans”, researchers found that there is a strong correlation between one’s MHC and their perfume choice. In the first experiment, participants were asked if they liked the smell or not. In a second experiment, participants were asked if they liked the smell, and if they wanted their mates to smell like that. From these experiments, they found out that people sharing specific MHC alleles also share preference for specific perfume odor. In other words, there was a strong correlation between MHC type and one’s preference for the perfume ingredients such as musk, rose, or cardamone. Although this research could not assess which odors were related to MHC, it provides the basis for studies that can test the relationship between the MHC and perfume in more detail. If we can find which odors are related to MHC, we can analyze what perfumes can attract potential mates. If so, we can wear perfumes to not only enhance our body odors, but also to attract our mates.
For more information, please see:
Janeway CA Jr, Travers P, Walport M, et al. Immunobiology: The Immune System in Health and Disease. 5th edition. New York: Garland Science; 2001. The major histocompatibility complex and its functions.
Milinski M, Cory I, Hummel T, Boehm T. 2013 Major histocompatibility complex peptide ligands as olfactory cues in human body odour assessment. Proc R Soc B 280: 20122889.
Milinski M, Wedekind C. 2001 Evidence for MHC-correlated perfume preferences in humans. Behav. Ecol. 12, 140–149.
Contributed by Jonathan Adcock, Hana Ahmed, Robert Bruner, Farhan Momin, Andrew Shibata
How Bitter Taste Works
Specialized bitter taste receptors are concentrated at the back of the tongue. Upon eating a bitter food, these receptors are activated, and and a signal is sent to to the brain that leads to the perception of a bitter taste. Bitter taste receptors are encoded by the TAS2R gene family. This family includes nearly 25 genes and psuedogenes (genes that are no longer functioning) that are concentrated in bundles on chromosomes 3, 5, and 7. Extensive studies have been performed in order to determine which molecules in bitter foods can activate these receptors. Scientists have found that many of the compounds that activate the bitter taste receptors are chemicals produced by plants. Many of these compounds were also found to be toxic and if consumed could lead to illness or death.
Our ancestors and other animals have not always been able to taste bitter foods. The bitterness sensation is thought to have evolved 200 million years ago. The prevalent hypothesis is that bitter taste evolved by random gene mutation events which caused the formation of the TAS2R gene family and the bitter taste receptors on the tongue that could bind to toxic chemicals. Animals possessing these mutations were able to taste toxins in their food. These toxins would have tasted bad to the animal, and thus, the animal would learn to avoid the toxic food in the future. Animals with the mutations that produce the TAS2R gene family would be be better adapted to their environment because they can avoid toxic and poisonous foods that could cause sickness or death in the animal. Animals not possessing these mutations would still be susceptible to ingesting naturally occurring poisonous chemicals. Because these animals have improved survivability in comparison to other animals without the TAS2R genes, animals that could taste bitter foods would be better able to reproduce and pass the functional TAS2R genes to their offspring, who in turn would have increased survivability, be better able to reproduce and pas the TAS2R genes to their offspring. Organisms possessing the TAS2R genes have a higher fitness than organisms that do not posses this gene family. Thus, the TAS2R gene family would have been selected for via natural selection and became the ability to taste bitter foods would have become dominant in the population.
This is especially true in the case of the thyroid-inhibiting toxin, PTC. PTC is known to decrease thyroid hormone, which regulates metabolic function. PTC can also lead to liver damage and a host of other medical problems that would eventually lead to death. Being able to taste the PTC toxin would have allowed our ancestors to to avoid toxic foods that if ingested would ultimately lead to their death. Because of this, the ability to taste the PTC toxin would be passed on to the next generation and contribute to the increased fitness of the following generation. In this way, the bitter taste genes would become selected for and would become prevalent in the population.
Although variation in taste facilitated the evolution of primates and other animals, in modern human society it can be detrimental. With the advent of agriculture, there is less need for tasting of bitter food. Highly nutritious vegetables are known to activate the bitter taste receptors. Instead of doing their intended evolutionary job of protecting from toxic materials, the bitter taste receptors are preventing some people from getting an adequate daily amount of nutritious vegetables due to their aversive taste.
Additionally, some individuals have extremely high sensitivity to bitter tastes resulting from higher rates of expression of the TAS2R gene. These individuals are known as “supertasters”. Supertasters can be found in the highest frequency in parts of Asia, Africa, and South America. This may be because these areas originally possessed a higher concentration of toxic plants and animals in comparison to other areas. In order to compensate for the increase in potential toxins, the individuals living in this area might have benefited more from bitter taste receptors. Today, many supertasters dislike a wide variety of vegetables such as cabbage and soy, and favor sweet items over bitter vegetables. This not only leads to increased chance of obesity and diabetes, but because of the avoidance of vegetables there is increased risk for GI diseases such as colon cancer. Not all side effects are bad though. Supertasters have a higher dislike for alcohol, carbonated beverages, and smoking. Avoidance of these items is actually quite beneficial in boosting heath.
Next time you don’t feel like eating your vegetables, you can blame it on evolution!
More Reading…
Campbell, M. C., P. A. S. Breslin, A. Ranciaro, S. A. Tishkoff, D. Drayna, D. Zinshteyn, G. Lema, T. Nyambo, J.-M. Bodo, S. Omar, J. Hirbo, and A. Froment. “Evolution of Functionally Diverse Alleles Associated with PTC Bitter Taste Sensitivity in Africa.” Molecular Biology and Evolution 29.4 (2012): 1141-1153.
Wooding, Stephen. “Evolution: A Study in Bad Taste?.” Current Biology 15.19 (2005): R805-R807.
Contributed by Sara Allison, Md Saon, Hassan Jassani, Siraj Quad
There is a general misconception that evolution has some sort of directionality associated with it where natural selection pushes organisms only to improve over time towards perfection. The misconception assumes that evolution only produces traits that the organism needs to survive and live long lives. This, however, is not entirely accurate, nor is it the whole story. Natural selection acts on random mutations and selects the ones that best help the organism to survive in a given environment or ones that increase its reproductive fitness. The traits selected for may not be perfect, but are good enough to be maintained through selective pressures. We will focus on a secondary sexual characteristic and sexual cannibalism as evidence for the fact that evolution is not perfect, in that there are not only benefits but also costs for these characteristics.
One example of a trait that is not perfect or optimal for the survival of the organism is the male rhinoceros beetle’s increased horn size. In general, males’ horns tend to be bigger than females’; females prefer males with bigger horns. This trait is not perfect because of the fact that bigger horned rhinoceros beetles experience increased predation, in spite of the trait’s evident advantage when it comes to sexual selection. Thus, the trait is advantageous because it helps males acquire mates and reproduce. However, it is also costly since males with bigger horns have an increased risk of predation. The reason this trait has been favored in spite of its imperfection is because the benefit of big horns being preferred by females outweighs the cost of increased predation through an increase in the number of offspring.
Figure A shows that the big horned male rhinoceros beetle has attracted the female beetle and has a high probability of mating with her—a benefit of big horns. Figure B shows that a smaller horned beetle has failed to attract the same female. Thus, Figure C shows this female fleeing from the small horned beetle without mating with him. Figure D shows that the big horned male receives more predatory attacks than the small horned beetle—a cost to having big horns.
Another example of imperfection in evolution is the evolution of sexual cannibalism, which is an extreme form of sexual conflict that involves the killing and consumption of the mate either before mating or after mating. It is possible that the occurrence of sexual cannibalism is influenced by low prey availability, which motivates the individual to eat its mate to obtain sustenance—this is known as the foraging hypothesis. Consequent benefits can include an increase in body mass, a healthier body condition, or increased reproductive ability. A study of the orb-web spider demonstrated that sexual cannibalism increases offspring survival, in which cannibalistic females produced offspring with longer survival times than females that were prevented from consuming their mate. Although there are benefits, there are also very significant costs. Eliminating the father means a definite loss of any potential paternal care. Additionally, cannibalism can occur before mating and, therefore, cause reproductive failure. In short, the evolution of sexual cannibalism comes with costs and benefits.
The evolution of the big horned male rhinoceros beetle and sexual cannibalism epitomizes the imperfect nature of evolution. Both traits are not perfect in that they come with significant costs. They are maintained because the benefits of each trait outweigh the costs.
For more information, see:
McCullough, Erin L., and Douglas J. Emlen. “Evaluating the costs of a sexually selected weapon: big horns at a small price.” Animal Behaviour 86.5 (2013): 977-985.
Wu, Lingbing, et al. “Factors influencing sexual cannibalism and its benefit to fecundity and offspring survival in the wolf spider Pardosa pseudoannulata (Araneae: Lycosidae).” Behavioral ecology and sociobiology 67.2 (2013):205-212.
Newman, Jonathan A, and Mark AElgar. “Sexual Cannibalism in Orb-Weaving Spiders: An Economic Model.” American Naturalist, The 138.6 (1991):1372-1395.