Rapid Evolution of Atlantic Tomcod due to Water Pollution by Toxic Chemicals

            Pollution is bad, we all know it. It’s bad for the human population and the environment in general, but pollution as a driving force for evolution is a relatively new concept. Over the past few decades, pollution has been a prominent driving force in the evolution of various species. For the Atlantic tomcod (Microgadus tomcod) of the Hudson River, water pollution caused by the improper disposal of toxic chemicals has led to rapid evolution, enabling the Atlantic tomcod to adapt to an environment heavily polluted by polychlorinated biphenyls (PCBs).

The dumping of PCBs in large bodies of water such as lakes and rivers was banned in the United States in 1977 [3]. Before its banning, the dumping of such toxic chemicals was overwhelming common as their use was prominent in the manufacturing sector [3]. In the Hudson River alone, over a million pounds of PCBs were released by General Electric during the two decades prior to its banning [2]. PCBs are long lasting chemicals due to their sedimentation in the soil and resistance to degradation [2]. They cause serious health issues in animals exposed to them, such as cancer, through their stimulation of the aryl hydrocarbon receptor (AHR), which is an important transcription factor [2]. PCBs bind to the AHR forming an active AHR-ligand complex that enters the nucleus and activates genes at the wrong time [2]. The most studied AHR is AHR2 due to it being the most active version in fish species [4].

The presence of PCBs in the Hudson River created a strong selection force against Atlantic tomcod expressing the normal AHR. This strong selection force combined with genetic mutation resulted in alleles expressing some form of PCB resistance to be favored, as individuals with PCB resistant phenotypes are capable of surviving and reproducing in this toxic environment [1]. The adaption to high levels of toxins takes on the form of an AHR2 that is two amino acids shorter than the AHR2 typically seen in fish, the result of a six base pair deletion [4]. This small change gives the receptor a significantly lower affinity for PCBs, preventing them from turning on genes that should not be activated [2][4].  

Figure 1. Overview of PCB Resistance through AHR Mutation [2]

Other fish from less polluted waters would not survive in the Hudson River due to them lacking the PCB resistant AHR. Take for instance the Atlantic tomcod populations of the Connecticut Niantic River and Shinnecock Bay in Long Island. In both of these populations the presence of this variant is small (~5%) whereas the presence of the variant in the Hudson River population is extremely high (99%), with the non-variant allele only observed in heterozygotes [4]. The low presence of this AHR2 mutant in other fish populations indicates that this variant is generally not favored, further confirming that the mutated AHR2 expressed in the Atlantic tomcod of the Hudson River was a result of fast adaption (<60 years) to extremely high levels of toxins in its environment [2].

While the Atlantic tomcod possesses immunity to the toxic effects of PCBs, the same cannot be said for the species higher up in the food chain as all species experience change at a different pace. What results is the passing of PCBs present in the fish to predators that may not possess resistance to PCBs. In such a manner, the water pollution caused by toxins has consequences that extend beyond its immediate effects on the Atlantic tomcod population. In an effort to reduce the pollution, General Electric is currently in the process of dredging out the contaminated sediment from the Hudson River [2][3]. As the mutated AHR is only favored in this specific type of environment, it is possible that the removal of the toxic chemicals will affect the fitness of the Atlantic tomcod of the Hudson River, resulting in another shift in the evolutionary pattern of this species.

-Mary Morales

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References:

[1]        Roy, N.K., S.C. Courtenay, R.C. Chambers, I.I. Wirgin. 2006. Characterization of the aryl hydrocarbon receptor repressor and a comparison of its expression in Atlantic tomcod from resistant and sensitive populations. Environmental Toxicology and Chemistry 25: 560-571.

[2]        “Toxic River means rapid evolution for one fish species.” 2011. Understanding Evolution. Web.  <http://evolution.berkeley.edu/evolibrary/news/110301_pcbresistantcod>.

[3]        “Waters of change.” 2011. The Economist. Web. <http://www.economist.com/node/21534749>.

[4]        Wirgin, I., N.K. Roy, M. Loftus, R.C. Chambers, D.G. Franks, M.E. Hahn. 2011. Mechanistic Basis of Resistance to PCBs in Atlantic Tomcod from the Hudson River. Science 331: 1322-1324

Urban Acoustic Pollution and Changing Birdsongs

            It comes as no surprise that New York City is a noisy place.  Cars are honking, people are yelling, and it seems like construction never ends.  However more than simply adding to the crabbiness of New Yorkers, these urban sounds are causing major wildlife concerns.  Noise pollution is one of the most prevalent yet also most overlooked causes of modern pollution.  New York City and other major metropolitan areas are overwhelmed by acoustic pollution and the animals, specifically songbirds, are being affected.  However, the songbirds of urban areas are changing their behaviors and passing their new songs on to the next generations.   Songbirds are changing with the changing environment, and it is because of acoustic pollution.

            Three recent studies have been conducted on the subject of songbirds and noise pollution and all have come to similar findings.  Birds that sing on a low frequency are unable to communicate with their young or with potential mates[1][2][3].  These studies were conducted with sparrows (Schroeder), the great tit (Halfwerk et al.), and a variety of urban oscines, or songbirds (Rios-Chelen et al.).  All of these studies found that their urban birds had difficulty when they sang at a low frequency because it was either matched or masked by the ambient noise pollution.

            However, these studies also noticed that birds were changing their songs to react to their environment.  The longer the bird communities were exposed to urban noise pollution, the higher the birdsongs became.  As Rios-Chelen explains, “song learning or song plasticity allows birds to achieve a greater adaptation of their songs to the acoustic conditions of the environment in which they live” ³.  These three studies universally found that birds with the capacity to learn a new, higher frequency song had higher fitness levels by being able to communicate with their young and with potential mates¹²³.

            These studies show evidence that the ability to adapt one’s birdsong is a genetic trait.  Some oscines, ones that apparently did not have the ability to adapt their songs on their own were also not able to copy the birdsongs of others².  Additionally, the ability to change a birdsong was found to be passed down through generations, with offspring of changed birds to have higher frequency songs and be able to increase their song frequencies¹.

            The sounds of urban areas are changing and that is causing urban songbirds to change.  Birds that are unable to change their songs to overcome acoustic pollution are both dying out and abandoning their young.  Only the birds that can change their tune and increase their song frequency are able to survive and mate.  No wonder people say it’s hard to be single in New York City.

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[1] Schroeder, J, Nakagawa, S, Cleasby C, Burke T (2012) Passerine birds breeding under chronic noise experience reduced fitness. PLoS ONE, 7: e339200. doi: 10.1371/journal.pone.0039200

[2] Halfwerk, W., Sander BOt, Jasper Buikx, Marco van der Velde, Jan Komdeur, Carel ten Cate, and Hans Slabbekoorn, Low-frequency songs lose their potency in noisy urban conditions, Preceedings of the National Academy of Sciences, v. 108 no. 35.

[3] Rios-Chelen, A.A., C.SaLaberria, I. Barbosa, C. Macias Garcia, and D. Gil, The learning advantage: bird species that learn their song show a tighter adjustment of song to noisy environments than those that do not learn, Journal of Evolutionary Biology, p. 2171-2180.

The Impact of Multiple Stressors On the Evolution and Survival of Natural Populations

With outbreaks of diseases and increased pollution in our environments, many natural populations just cannot get a break. These organisms are exposed to many different stressors, whether biotic (such as predation or parasites) or abiotic (such as chemical pollution or losses of habitats). These stressors can yield genetic adaptations in organisms due to strong selection pressures from their local habitat, of course if gene flow is negligible. (Coors et. al. 2009) When threats such as parasites, pollution, or predation, are present in an environment alone, populations are able to react to each in a different induced specific adaptation. However, when it comes to multiple stressors, evolution has been proven to play a part.

One recent experiment highlights what happens when organisms are exposed to multiple threats and its effect on an individual’s fitness. In this experiment, when the model organism Daphnia magna is introduced into an environment with both parasites and pesticides, the populations either adapt to one set of conditions or the other. D. magna has been chosen as the model organism due to its ability to produce latent egg stages that can be conserved. The D. magna clones from these latent eggs are exposed to Pasteuria ramosa (parasite) and diazinon (insecticide). After the exposure, each organism was tested for infections, survival rate, and the number of offspring for 21 days. The results showed that both of these stressors caused higher mortality rates in the D. magna populations together than if they were in contact with just one. Moreover, it was found that the evolution to repel one stressor, such as the diazinon, lowered resistance against another stressor, such as P. ramosa. However, it must be noted that by the end of the 3 weeks of the experiment, there were no observable signs of parasitic infection within any of the population, but there was a drastically higher mortality rate when the D. magna were exposed to both the pesticide and the parasite simultaneously instead of one stressor by itself. (Jansen et. al. 2011)

This evolutionary catch-22 could be due to a number of factors. For example, the P. ramosa could be causing an immune suppression within the population that allows other disturbances, in this case the diazonin, to easily infiltrate the populations. On the other hand, the increased mortality due to multiple disturbances could be a result of the accumulation of the increasing demand for energy by each of the stressors.  In addition, there are three different reasons for why there were no visible signs of parasitic infections even though it still played a huge part in the survival rate of the hosts. First, it could be that the hosts were infected by certain spores that were not virulent for these set of clones. Secondly, it could be that the specific strain of P. ramosa chosen was not infectious for the hosts. This could be because the infectiousness of a parasite, its influence on the host’s ability to survive and reproduce, is dependent on how a specific host and parasite interact and can also be impacted by the conditions of its environment. (Coors et. al. 2008)  Last, there is a possibility that due to unknown causes the amount of viable spores declined. Nevertheless, infected or uninfected, the parasites caused a lot of stress on the survival rates of these hosts. (Buser et. al. 2012)

Diazonin, often used for agricultural and domestic purposes, can cause death, immobilisation, delay in reproduction, and less offspring yield, because of its ability to suppress acetylcholinesterase, a crucial enzyme of the nervous system.  Toxic pollutants such as diazonin can cause genotoxicity or genetic bottlenecks and can therefore have long term effects on the genetic structure of a population. P. ramosa, the parasite, was a great parasite to use because detection of its infection was clear. Once D. magna was infected by the parasite, the individuals would become infertile, and its body would change in appearance – it would grow larger and darker. This parasite would be released after the death of its host in the form of spores and could remain inside the sediments of its aquatic environment and continue being infective for many years after. Thus, having to deal with two such strong population disturbances has led to an adaptation struggle as it is difficult to keep defences against both. . (Buser et. al. 2012)

In conclusion, our society’s tendency to contaminate our environment is having a dramatic impact on the natural populations that habituate them. Each population of organisms already have their own natural predators and problems that they have to surpass in order to survive and reproduce, not counting the ones humans impose on them. Such as in the experiment above, adapting to combat parasitic or predation threats is lowering population’s resistance against pollution and causing very low survival rates. The anthropogenic stressors that humanity inflicts on these populations are the last and ultimate blow that is making it difficult for them to progress and flourish in today’s world.

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References

Buser, C.; Jansen, M.; Pauwels, K.; de Meester, L.; & Spaak, P. (2012). Combined exposure to parasite and pesticide causes increased mortality in the water flea Daphnia. Aquatic Ecology. DOI: 10.1007/s10452-012-9397-9

Coors, A.; Decaestecker, E.; Jansen, M.; & de Meester, L. (2008). Pesticide exposure strongly enhances parasite virulence in an invertebrate host model. Oikos DOI: 10.111/j.1600-0706.2008,17028.x

Coors, A.; Vanoverbeke, J.; de Bie, T.; & de Meester, L. (2009). Land use, genetic diversity and toxican tolerance in natural populations of Daphnia Magna. Aquatic Toxicology. DOI: 10.1016/j.aquatox.2009.08.004

Jansen, M., Stoks, R., Coors, A., van Doorslaer, W., & de Meester, L. (2011). Collateral damage: Rapid exposure-induced evolution of pesticide resistance leads to increased susceptibility to parasites. Evolution DOI: 10.1111/j.1558-5646.2011.01331.x

Steel Mill Pollutants Re-shaping the Entire Genome: Possibility

Air pollution this, air pollution that. We all know about it when mentioned in small talks about respiratory problems (Davis, 2002), but hardly anyone goes out of one’s way to do something about it. What if, some of these air pollutants were found to induce a more profound change - heritable DNA mutations, for example - that could forever change your generation’s genome? Freaky.

A study was conducted in Hamilton Harbor and Lake Ontario to test air pollutants produced from steel mills nearby. A rural reference point 30 km away from the immediate-polluted areas was chosen to serve as a control. An equal number of fecund male and female mice were picked at random and were exposed to the three sites (rural-pristine, Hamilton, and Lake Ontario) for 10 weeks (Somers et al. 2002) They were brought into the lab for their own DNA analysis and their reproducibility, to observe any effects on DNA of future generations.

The results were shocking in the least. They discovered that the paternal germline was significantly affected by the mutagens closer to the polluted area, while the maternal germline was not significantly affected. Male germ cells that have not yet gone through meiosis were shown to be sensitive to airborne emissions near steel mills. This study was only conducted for 10 weeks, and the significantly elevated mutation rate is in every aspect a reason for concern. Globally, hundreds of thousands of humans live or work in industrial areas near steel mills and are incidentally or intentionally exposed to airborne emissions. Whether workers or innocent bystanders, they might be at risk of increased heritable mutation through exposed fathers. Of course, there should be a more thorough investigation of the genetic hazards associated with exposure (whether incidental or occupational) to contaminated air in urban and industrial areas, but it is never foolish to take precautions.

References:

Somers, C., Yauk, C., White, P., Parfett, C., Quinn, J. “Air pollution induces heritable DNA mutations.” PNAS 99(25): 15904-15907. 10 Dec. 2002. 

Davis, M. "Recessions and Health: The Impact of Economic Trends on Air Pollution in California." American Journal of Public Health 102:10, 1951-1956. 2002. 

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Evolution of A. stolonifer and A. tenuis due to Aerially Borne Metals

Mining metals has been a crucial activity since the beginning of the Industrial Revolution; it has supplied countries with bullets, supplies, and utensils for two world wars and has renovated our transportation systems. All of the processes, such as crushing, grinding, washing, smelting, etc., result in significant volumes of waste being deposited in the soil, water, and air surrounding the mining site. It is estimated that per year the median values of worldwide metal deposits for Cd, Cu, Pb, and Zn are 22, 954, 796, and 1372 10^6 kg (Sheoran 2011). Mining sites can be found in many locations, including Albania, Bulgaria, Finland, Spain, Canada, and the United States of America. Most metals, like Copper, remain near the mining site but can be found up to 33 km away. Others, such as Arsenic may travel longer distances due to its “atmospheric residence time” (Yoon et al. 2012). The vegetation and animal life that surround mining areas has been drastically effected by the toxic metal pollution; loss of biodiversity is expected near these areas.

            

However, there has been significant research that shows copper tolerance evolving in plant populations exposed to aerially borne waste from mines. Copper metal is normally toxic to plants in low concentration and thus, has resulted in changes to their genetic structure. A metal refining industry in SW Lancashire emits dust particles of copper into the surrounding environment resulting in soil copper levels of up to 4,000 ppm (Nature 1972). While in some places the vegetation has been completely destroyed, the grassland that does exist includes Agrostis stolonifera and Agrostis tenuis. The observed structures of A. stolonifera in the areas surrounding the mine are extremely different depending on the ground age. Older grassland in highly contaminated areas has a continuous cover despite the high metal levels. In lawns replaced within the past 10 years there is serious contamination yet no plant life (Nature 1972).  It appears that the new plants that were introduced into the new lawns could not handle the high levels of metal toxins. In contrast, the older grassland had selected towards copper-tolerant individuals and had disposed of weak genotypes, or non-tolerant/slightly tolerant genotypes. This is a clear example of recent evolution and natural selection of plant species due to the pollutant of aerially borne metals.

References:

Kabir, Ehsanul, Sharmila Ray, Ki-Hyun Kim, Hye-On Yoon, Eui-Chan Jeon, Yoon Shin Kim, Yong-Sung Cho, Seong-Taek Yun, and Richard J. C. Brown. "Current Status of Trace Metal Pollution in Soils Affected by Industrial Activities."National Center for Biotechnology Information. U.S. National Library of Medicine, 03 May 2012. Web. 19 Feb. 2013. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3356731/>.

Sheoran, V., P. Poonia, and S. K. Trivedi. "Metal Pollution in Soil and Plants Near Copper Mining Site." International Journal of Geology, Earth and Environmental Sciences 1.1 (2011): 27-34. Web. 18 Feb. 2013. <http://www.cibtech.org/J%20GEOLOGY%20EARTH%20ENVIRONMENT/PUBLICATIONS/2011/Vol%201%20No.%201/016-4-JGEE-SHEORAN.pdf>.

Wu, Lin. "Aerial Pollution and the Rapid Evolution of Copper Tolerance." Nature 238 (1972): 167-69. Nature. Web. 17 Feb. 2013. <http://www.nature.com/nature/journal/v238/n5360/pdf/238167a0.pdf>.

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Chernobyl: Radiation’s Impact on Biodiversity

Oil spills. Burning fossil fuels. Dumping chemical waste. Littering. These are the things that we are taught endanger the natural world every Earth Day. From a young age, we learn about the perils of discarding our waste into natural ecosystems. But some dangers are not as obvious. Radiation cannot be seen, but it has a dramatic effect on any ecosystem that is affected by it. One of the most profound examples of this phenomenon is Chernobyl. Over twenty years after the reactor meltdown, I could only imagine that the landscape would be barren of life except for those microorganisms that had managed to feed on whatever remained after the incident. I could not be more wrong.

Biodiversity has only increased since the Chernobyl disaster. Research conducted by James Morrison of the University of South Carolina shows that nature as a whole is actually thriving¹. In fact, many of the species that exist there now, such as bears and wolves, did not before the reactor failed, and the presence of these apex predators indicates that many other species must be surviving in order to maintain the food chain². It is hypothesized that these organisms have developed more efficient ways of dealing with radiation damage. Only those individuals that can cope with the conditions make it to adulthood, eliminating those most highly affected by the radiation³. Some species of fungi have even demonstrated increased fitness in the presence of radiation⁴.

But this is not to say that we should begin irradiating all of our natural ecosystems. Humans and some animals such as birds are particularly vulnerable to the effects of radiation. Some bird species have demonstrated a distinct increase in juvenile mortality⁵. Morrison makes it very clear that such effects would also translate to humans who would suffer from significantly shorter life spans and a similarly increased infant mortality rate⁶. While nature as a whole may be able to combat the damages humans cause with radiation, humans would be unlikely to survive in such hostile conditions.

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 ^1,2,3,5,6http://www.nature.com/news/2005/050808/full/news050808-4.html

⁴ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2677413/