Introduction
The Atlantic tomcod, biologically known as the Microgadus tomcod, is native to the coasts of North America and Canada, where it is popular with fishermen, especially between December and February when it is in season. It mostly lives in brackish coastal or freshwater, which makes it a common inhabitant of rivers and landlocked lakes. Its diet, for the most part, consists of crustaceans, worms and other small water creatures.
Background
What sets this species of fish apart from most other aquatic animals is the speed with which it evolved in the last half century, enabling it to survive the effects of perennial human water pollution. From the late 40s to early 90’s, the Hudson River, one of the biggest natural habitats for the tomcod, was contaminated with over a million pounds of polychlorinated biphenyls (PCBs) from industrial installations (Klauda, Thomas and Gary 831). Consequently, thousands of fish and other creatures living in these waters died, resulting in an acute natural imbalance. However, instead of dying out as expected, the tomcod begun to thrive, even in the high concentration of toxic chemicals (Dybas). Initially, they died just like other fish from a series of chemical related disorders especially heart defects in juveniles. As a result, most of the fish hatched after the contaminating event were gradually eliminated leaving only a few survivors. However, after a few decades, they appeared to have developed immunity to the effects of the poison, which motivated biologists to investigate their coping mechanism (Wirgin et al. 1322). Newly hatched fish showed no outward signs of heart defects even after the near depletion of some of the other species from the same problem. Scientists discovered that, despite their continued survival, the levels of PCBs in their blood were the highest in nature (Klauda, Thomas and Gary 833). In fact, for any other fish, even a fraction of the tomcod’s PCB blood levels would have been be lethal.
It later emerged that they underwent extremely rapid evolution, which allowed them to modify some of the proteins in their DNA and regulate the toxicity of PCBs. As a result, it became difficult for toxins to bind to their receptors, making them ineffective against the tomcod (Wirgin et al. 1323). Studies of the small fish in different rivers have shown that this mutation is mostly limited to the Hudson, although, there are some other parts of the US, such as the Niantic River in Connecticut, where a similar mutations have been observed. Scientists argue that the tomcod must have inbuilt mechanisms for mutation, which are triggered whenever they are faced with chemical pollutants (Yuan et al. 78). The process of natural selection occurs when organisms that are unable to survive in a given environment are allowed to die out, while those with suitable adaptive genes reproduce and replace them. Through this process, a species can protect itself from extinction by only retaining the fittest to breed future threat-resistant generations. The tomcods’ evolution followed the law of natural selection in that, the hatchlings of the fish without the mutating gene died. Conversely, those with the gene survived and passed it on to their young, making them immune to the toxins in the water and ultimately creating a generation of PCB resistant tomcod. As a result, with each successive generation, the non-mutant fish were “weeded” out ensuring that their genes could not contaminate the surviving fish by breeding with them. The mutation is however only useful for the tomcod’s survival since, when other animals feed on them they suffer the ill effects of PCBs (Dybas). I chose to study these organisms since the mutations they employ to deal with chemical toxins are similar to the adaptations of various human and animal bacteria to antibiotic treatment. Therefore, understanding the evolution of the tomcod may be useful in discovering new knowledge in pharmacy and medicine, especially concerning antibiotic-resistant organisms. In addition, they provide a unique opportunity to watch the process of evolution as it happens since it typically takes thousands of years for animals to develop such mutations. Although some critics have opposed the application of Darwinism to tomcod evolution, their changes, are nonetheless, directly connected to the process of natural selection. The rapid evolution of tomcod can also be compared to another, “live” evolution process involving the African elephants, which are losing their tusks, apparently, to protect themselves from poachers. The tomcod, therefore, provides one with invaluable insight in the field of evolution by acting as an accessible, verifiable example.
Hypothesis
While the tomcod’s adaptation has been found to be very useful in surviving toxic waters, it has been suggested that these evolutionary traits, by virtue of their rapid nature may not be sustainable. If the Hudson mutants were relocated to an environment where they are not exposed to PCBs, they might not survive and would need to mutate once again to adjust to clean water. The rapid evolution, according to some scholars is only a temporary measure in response to a temporary problem. Therefore, when the river is clear of toxic waste in the future, they will likewise readjust their DNA through natural selection. The fish that need PCBs to survive, as a result of the initial mutation will die out, and “normal” tomcod will once again populate the Hudson River. The hypothesis for the experiment outlined later in this paper will address the ability of the tomcod’s rapid evolution to reoccur in a situation where the factors that sparked it off are absent. Therefore, I propose that, if tomcod were removed from the Hudson River, or if the river eventually became chemical free, it would have the same effect poisoning the river had on original non-mutant fish.
The Experiment
Testing this hypothesis will require recreating conditions similar to the ones that would occur if Hudson tomcod were forced to live in PCB free water. To do this, I would first obtain samples of the fish from the Hudson River and introduce them into a PCB free water system, in either a fishpond or a restricted part of their natural habitat for observation. As a control experiment, I would also move the same number of fish from the Hudson to the Niantic where similar mutations have been observed. Once again, this would be in a controlled system to allow tracking and observation. I would then study samples in both areas, following their gestation periods and collecting data on how they react and adapt to the new environments. Since the original mutations took place over several decades, I would ensure I have introduced enough fish in the new areas to create space for natural selection. With each new generation of fish, I would collect some samples and test them to find out if the mutations that allowed them to survive the PCB poisoning are still present and if they are undergoing any genetic change. The samples collected will taken to a laboratory for dissection and biopsies will be collected from their tail fins, where evidence of PCB poisoning is most obvious due to accumulation. For these tests, the DNA from the samples will be isolated to determine the presence and levels of PCB related mutations. The process will require a QUIAGEN DNA kit to purify the DNA material collected and then using alcohol precipitation, I will form DNA pellets and re-suspend them in a Hydration solution. I will then read the different samples using a Nanodrop spectrophotometer to establish the PCB levels and the purity of the DNA. The data collected from the tomcod in the “clean” river and the control setting will be used to create a statistical analysis, which will guide me in making various inferences on the effects of PCB free water on their rapid evolution. I will also record statistics on the fish population and their mortality rates with special emphasis on anything associated with heart or liver problems, since these are the main manifestations of PCB poisoning. I would then use the information gathered to establish the extent of the changes occurring in both environments and determine if indeed Hudson River Atlantic tomcod can survive in clean water without backward evolution. If they do, it will mean they have successfully evolved sufficiently to live in both polluted and unpolluted environments, a fact that most scientists involved in their study have dismissed as unlikely.
Works Cited
Dybas, Cheryl L. “Toxic Waters Provide a Snapshot of Evolution.” The Washington Post 23 Jan. 2006. Web. 4 March. 2015.
Klauda, Ronald J., Thomas H. Peck, and Gary K. Rice. “Accumulation of polychlorinated biphenyls in Atlantic tomcod (Microgadus tomcod) collected from the Hudson River estuary, New York.” Bulletin of environmental contamination and toxicology 27.1 (1981): 829-835. Print.
Wirgin, Isaac, Nirmal K. Roy, Matthew Loftus, R. Christopher Chambers, Diana G. Franks, and Mark E. Hahn. “Mechanistic basis of resistance to PCBs in Atlantic tomcod from the Hudson River.” Science 331, no. 6022 (2011): 1322-1325. Print.
Yuan, Zhanpeng, et al. “Evidence of spatially extensive resistance to PCBs in an anadromous fish of the Hudson River.” Environmental health perspectives (2006): 77-84. Print.