Population Genetics Lab
by Satya Sheftel-Gomes ('19)
Abstract
In this lab, we investigated the question of how genetic variants spread through populations of people. More specifically, we tracked how time and environmental factors changed rates of Sickle cell gene frequency within a set population. To do so we plugged in numbers into parameters given by the simulation, Simbio Virtual Labs. Then we would track the frequency of the HBS and HBA Alleles over time, through a live graph. In conclusion, we found that in very wet climates that held many mosquitos, and thus provided an ideal climate for malaria, the percentage of people within a certain population with sickle cell anemia was much higher for a consistent amount of time then in dry climates without the presence of malaria.
Introduction
In the Science and Origins of Race and Gender class, we are learning to debunk the historical theories of surrounding race and gender using science and historical arguments. Last week, we read two articles, “A Family Tree in Every Gene,” by Armand Marie Leroi and “Confusions about Human Races,” by R.C. Lewontin, concerning the role science plays in the legitimacy of categorizing humans by “race.” A topic of interest for both authors was the role of race in medicine, Leroi arguing that recognizing the science of race was important for medicine given “Different races are prone to different diseases,” while Lewontin argued that it wasn’t race that was the influential variable, it was ancestry. In this lab we investigated how genetic variants, specifically the Sickle Cell Anemia gene, spread in human populations in Africa depending on the probability of Malaria. Sickle Cell Anemia is an allele of the hemoglobin gene made up of either single or double S (sickle traits). HbS, or the sickle cell allel, causes abnormal hemoglobin which leads to red blood cells being sickly and oddly shaped. Malaria is a disease caused by a protist that lives in mosquitos. When a mosquito bites a human, the malaria parasite travels through the bloodstream to the liver, where it settles among healthy red blood cells. Through our investigation, we will be able to find out if sickle cell anemia is truly a “black” disease, as was pointed out by Leroi, or if it is ancestry from a Malaria prone environmental zone that creates that belief, which while get us further in the class’ agenda to invalidate the notions of human biological difference by race.
Method
In this lab we used “Simbio Virtual Labs,” an electronic simulation that, depending on the applied variables, graphs evolutionary phenomenons on a live graph. To do this Lab, we opened the Simbio Virtual Lab application and clicked on the “Evobeaker Lab: Sickle Cell Alleles.” Before running any trials we set parameters for both Sickle Cell Anemia Death Rate and Initial Number of Sickle Cell Carriers, to 60 and 20 respectively. Then for the first trial, we selected “Dry/no mosquitos” under Moisture, Mosquitoes, and Malaria in Africa. We then ran the data by pressing Go in the controls settings, recording for 100 years. After 100 year press stop and screenshot the graph. Then repeat, plugging in all the same data except the environment, which you should change to “very wet/many mosquitos” under Moisture, Mosquitoes, and Malaria in Africa.
Data
In this lab, we investigated the question of how genetic variants spread through populations of people. More specifically, we tracked how time and environmental factors changed rates of Sickle cell gene frequency within a set population. To do so we plugged in numbers into parameters given by the simulation, Simbio Virtual Labs. Then we would track the frequency of the HBS and HBA Alleles over time, through a live graph. In conclusion, we found that in very wet climates that held many mosquitos, and thus provided an ideal climate for malaria, the percentage of people within a certain population with sickle cell anemia was much higher for a consistent amount of time then in dry climates without the presence of malaria.
Introduction
In the Science and Origins of Race and Gender class, we are learning to debunk the historical theories of surrounding race and gender using science and historical arguments. Last week, we read two articles, “A Family Tree in Every Gene,” by Armand Marie Leroi and “Confusions about Human Races,” by R.C. Lewontin, concerning the role science plays in the legitimacy of categorizing humans by “race.” A topic of interest for both authors was the role of race in medicine, Leroi arguing that recognizing the science of race was important for medicine given “Different races are prone to different diseases,” while Lewontin argued that it wasn’t race that was the influential variable, it was ancestry. In this lab we investigated how genetic variants, specifically the Sickle Cell Anemia gene, spread in human populations in Africa depending on the probability of Malaria. Sickle Cell Anemia is an allele of the hemoglobin gene made up of either single or double S (sickle traits). HbS, or the sickle cell allel, causes abnormal hemoglobin which leads to red blood cells being sickly and oddly shaped. Malaria is a disease caused by a protist that lives in mosquitos. When a mosquito bites a human, the malaria parasite travels through the bloodstream to the liver, where it settles among healthy red blood cells. Through our investigation, we will be able to find out if sickle cell anemia is truly a “black” disease, as was pointed out by Leroi, or if it is ancestry from a Malaria prone environmental zone that creates that belief, which while get us further in the class’ agenda to invalidate the notions of human biological difference by race.
Method
In this lab we used “Simbio Virtual Labs,” an electronic simulation that, depending on the applied variables, graphs evolutionary phenomenons on a live graph. To do this Lab, we opened the Simbio Virtual Lab application and clicked on the “Evobeaker Lab: Sickle Cell Alleles.” Before running any trials we set parameters for both Sickle Cell Anemia Death Rate and Initial Number of Sickle Cell Carriers, to 60 and 20 respectively. Then for the first trial, we selected “Dry/no mosquitos” under Moisture, Mosquitoes, and Malaria in Africa. We then ran the data by pressing Go in the controls settings, recording for 100 years. After 100 year press stop and screenshot the graph. Then repeat, plugging in all the same data except the environment, which you should change to “very wet/many mosquitos” under Moisture, Mosquitoes, and Malaria in Africa.
Data
The Relationship Between Allele Frequencies, Time and a High Malaria Probability.
The Relationship Between Allele Frequencies, Time and a Low Malaria Probability.
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Caption: In this graph the percentage of HbS, starts low but within about 30 years spikes and stays at a consistent rate of a little under 50% of the population. This means that a little under 50% of the people within this set population carried the sickle cell gene for a constant rate after about 30 years, among a Malaria friendly environment..
Caption: In this graph the percentage of HbS starts low but stays consistent, not growing passed 8% of the population. This means that with low malaria probability, the percentage of people with sickle cell anemia stayed low consistently. |
Discussion
We investigated this lab to provide further insight on the points argued by Leroi and Lewontin regarding race and its importance to medicine. While Leroi argued that diseases like Sickle Cell Anemia are “black” diseases, Lewontin brings up a more nuanced argument that lays in geographical ancestry. Through this investigation, we were able to directly test these two arguments, using data to demonstrate the relation between race and medicine directly. In the first trial, where the relationship between allele frequencies, time and low malaria probability were tested, the initial frequency of the HbS gene was around 8% of the population. Over the next 100 years, it decrease to be around a consistent 4% of the population. In the second trial, where the relationship between allele frequencies, time and high malaria probability were tested, the initial frequency of the HbS gene was around 8% of the population. Over the next 100 years, it grew to be around a consistent 40% of the population. Considering those trials, it is obvious that Malaria probability relates greatly to the frequency of the Sickle Cell gene– without Malaria, the Sickle Cell Gene remains present in a very small part of the population, whereas with Malaria the Sickle Cell Gene spikes and stays at a fairly high, relatively constant rate. Given our knowledge of both Malaria and the Sickle cell gene, it is safe to say that Malaria cannot survive wellin Host bodies who carry the Sickle cell gene. The Malaria parasite travels through the bloodstream to the liver, where it engages with healthy red blood cells, and carriers of the Sickle Cell gene do not have many health red blood cells. Given that typically, Malaria is more deadly than Sickle Cell Anemia, people without the sickle cell gene who contract Malaria die, causing the majority of “healthy” or malaria free people in a given population to be HbS carriers. Now, the most environmentally ideal places for Malaria habitats are in wet places around the equator. That means much of Central Africa and India, and parts of South America and the Pacific Islands.
We investigated this lab to provide further insight on the points argued by Leroi and Lewontin regarding race and its importance to medicine. While Leroi argued that diseases like Sickle Cell Anemia are “black” diseases, Lewontin brings up a more nuanced argument that lays in geographical ancestry. Through this investigation, we were able to directly test these two arguments, using data to demonstrate the relation between race and medicine directly. In the first trial, where the relationship between allele frequencies, time and low malaria probability were tested, the initial frequency of the HbS gene was around 8% of the population. Over the next 100 years, it decrease to be around a consistent 4% of the population. In the second trial, where the relationship between allele frequencies, time and high malaria probability were tested, the initial frequency of the HbS gene was around 8% of the population. Over the next 100 years, it grew to be around a consistent 40% of the population. Considering those trials, it is obvious that Malaria probability relates greatly to the frequency of the Sickle Cell gene– without Malaria, the Sickle Cell Gene remains present in a very small part of the population, whereas with Malaria the Sickle Cell Gene spikes and stays at a fairly high, relatively constant rate. Given our knowledge of both Malaria and the Sickle cell gene, it is safe to say that Malaria cannot survive wellin Host bodies who carry the Sickle cell gene. The Malaria parasite travels through the bloodstream to the liver, where it engages with healthy red blood cells, and carriers of the Sickle Cell gene do not have many health red blood cells. Given that typically, Malaria is more deadly than Sickle Cell Anemia, people without the sickle cell gene who contract Malaria die, causing the majority of “healthy” or malaria free people in a given population to be HbS carriers. Now, the most environmentally ideal places for Malaria habitats are in wet places around the equator. That means much of Central Africa and India, and parts of South America and the Pacific Islands.
Western scientists, alike to the ones Leroi was referencing, analyze Sickle Cell Anemia as black disease due to multiple factors. First, because of the Malaria presence in the previously mentioned zones, Sickle Cell Anemia thrives in those geographical locations specifically, and as shown in our graphs, HbS carriers make up an abnormally large amount of the population in those areas. Second, because of the Atlantic slave trade, the majority of Black people in the Western world come from Central Africa, a highly wet, hot and Malaria friendly environmental zone. As a slave, you must have been healthy to receive a high price, so Malaria infected people were not traveling to the new world, while healthier, largely immune, sickle cell gene carriers were systematically shipped off. That means the majority of the Black population in western societies do likely carry the HbS gene, but not because they are Black, but because of their geographical ancestry. Take some examples, for instance, a native African person from South Africa has a extremely low chance of having the sickle cell gene, but they are still considered a racially “black” person. Their race has little to do with the diseases they carry. Another example, take white europeans. White europeans have almost no chance of having the sickle cell gene, because their environment is not conducive to Malaria, and therefore the sickle cell gene would’ve died out within 100 years, as is shown in trial 1.
Citations:
Malaria. (2017, March 17). Retrieved from https://www.cdc.gov/malaria/about/distribution.html
Citations:
Malaria. (2017, March 17). Retrieved from https://www.cdc.gov/malaria/about/distribution.html