3. The ILRN gene encodes a protein that acts as an antagonist to interleukin receptors. This gene hasthree alleles represented as A*1, A*2, and A*3. In a study on the relationship between genotype andchronic pain sensitivity, data was collected on the ILRN genotype of 100 people as follows:50A*1/A*126A*1/A*24A*1/A*310A*2/A*2A*2/A*3A*3/A*3010A. Calculate the frequency of each allele.B. Determine how many people there would be of each genotype if the population were in Hardy-Weinberg equilibrium and use the Chi-squared test to evaluate how well these expectation fit theobserved data

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Description: 3. The ILRN gene encodes a protein that acts as an antagonist to interleukin receptors. This gene hasthree alleles represented as A*1, A*2, and A*3. In a study on the relationship between genotype andchronic pain sensitivity, data was collected on t

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3. The ILRN gene encodes a protein that acts as an antagonist to interleukin receptors. This gene has three alleles represented as A*1, A*2, and A*3. In a study on the relationship between genotype and chronic pain sensitivity, data was collected on the ILRN genotype of 100 people as follows: 50 A*1/A*1 26 A*1/A*2 A*1/A*3 4 10 0 10 A. Calculate the frequency of each allele. B. Determine how many people there would be of each genotype if the population were in Hardy- Weinberg equilibrium and use the Chi-squared test to evaluate how well these expectation fit the A*2/A*2 A*2/A*3 A*3/A*3

3. The ILRN gene encodes a protein that acts as an antagonist to interleukin receptors. This gene has three alleles represented as A1, A2, and A3. In a study on the relationship between genotype and chronic pain sensitivity, data was collected on the ILRN genotype of 100 people as follows: 50 A1/A1 26 A1/A2 A1/A3 4 10 0 10 A. Calculate the frequency of each allele. B. Determine how many people there would be of each genotype if the population were in Hardy- Weinberg equilibrium and use the Chi-squared test to evaluate how well these expectation fit the A2/A2 A2/A3 A3/A*3

Biology: The Unity and Diversity of Life (MindTap Course List)

14th Edition

ISBN:9781305073951

Author:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Publisher:Cecie Starr, Ralph Taggart, Christine Evers, Lisa Starr

Chapter13: Observing Patterns In Inherited Traits

Section: Chapter Questions

Problem 4GP

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1. The first genetic test used a short DNA sequence that was closely linked to the Huntington’s locus. People taking the test were classified as to whether they had the DNA sequence that was linked to the Huntington’s disease. This method was 95% accurate. This means that 95% of the people who had the Huntington’s-linked DNA sequence actually inherited the Huntington allele. It also meant that 95% of the people who did not have the DNA sequence linked to the Huntington allele did not inherited the wild-type allele (not the Huntington allele).Why might this preliminary test not be as accurate as a gene test for the actual Huntington’s allele? Explain.
1. There are two different variations at STR locus THO1. Where did these variations come from? b) The STR locus D21S11 only has one variation. Why?
Alzheimer’s is a progressive neurological disorder resulting in dementia and memory loss that occurs in 10% of the US population older than 65. In the 1990s, several researchers showed evidence that the allele of a cholesterol precursor gene, APO E4, increased risk of developing the disorder compared to APO E2 or APO E3. This was especially pronounced if patients carried two alleles of APO E4. However, not all people with APO E4 develop the disorder and some without it will present with Alzheimer's nevertheless. This suggests other genes influence development of the disease. Current research has elucidated dozens of genes that interact with APO E4 pathways in hundreds of ways. As many as 27 of the interactions are epistatic, with some as dominant epistasis and some as recessive epistasis. In addition, some of the gene candidates for non-APO E4 Alzheimer’s have other relationships such as dominant, codominant or incomplete dominant. No reliable cure currently exists for Alzheimer’s…
Alzheimer’s is a progressive neurological disorder resulting in dementia and memory loss that occurs in 10% of the US population older than 65. In the 1990s, several researchers showed evidence that the allele of a cholesterol precursor gene, APO E4, increased risk of developing the disorder compared to APO E2 or APO E3. This was especially pronounced if patients carried two alleles of APO E4. However, not all people with APO E4 develop the disorder and some without it will present with Alzheimer's nevertheless. This suggests other genes influence development of the disease. Current research has elucidated dozens of genes that interact with APO E4 pathways in hundreds of ways. As many as 27 of the interactions are epistatic, with some as dominant epistasis and some as recessive epistasis. In addition, some of the gene candidates for non-APO E4 Alzheimer’s have other relationships such as dominant, codominant or incomplete dominant. No reliable cure currently exists for Alzheimer’s…
Alzheimer’s is a progressive neurological disorder resulting in dementia and memory loss that occurs in 10% of the US population older than 65. In the 1990s, several researchers showed evidence that the allele of a cholesterol precursor gene, APO E4, increased risk of developing the disorder compared to APO E2 or APO E3. This was especially pronounced if patients carried two alleles of APO E4. However, not all people with APO E4 develop the disorder and some without it will present with Alzheimer's nevertheless. This suggests other genes influence development of the disease. Current research has elucidated dozens of genes that interact with APO E4 pathways in hundreds of ways. As many as 27 of the interactions are epistatic, with some as dominant epistasis and some as recessive epistasis. In addition, some of the gene candidates for non-APO E4 Alzheimer’s have other relationships such as dominant, codominant or incomplete dominant. No reliable cure currently exists for Alzheimer’s…
1) What does these results mean as shown in the three graphs and t-tests? 2) Can you explain why these three graphs and t-tests ended up with these results? 2) How could someone improve on this study using the graphs and t-tests? If other scientists did this study is there something to recommend to them? 3) What variables were not considered in the graphs and t-tests that should be?
1. a) If you were at risk of a fatal disease such as Huntington’s disease and only the 95% accurate preliminary genetic test was available, would you take the test? After all, 95% of the time the test would tell you whether you would eventually get Huntington’s disease or whether you did not have to worry about getting this disease. b) The linkage distance between the DNA sequence used in the test and the actual Huntington’ disease locus was 5%. In a large sample of the Venezuelan family, what percentage of people would inherit the DNA sequence but not the Huntington’s allele (i.e. be a false positive test for Huntington’s)? What percentage of that large Venezuelan family would not inherit the DNA sequence but would inherit the Huntington’s allele (i.e., be a false negative test for Huntington’s)?
1. The compound phenylthiocarbamide (PTC) tastes very bitter to most persons. The inability to taste PTC is controlled by a single recessive gene. In the American white population, about 70% can taste PTC while 30% cannot (are non-tasters). Estimate the frequencies of the Taster (T) and nontaster (t) alleles in this population as well as the frequencies of the genotypes
According to the tables, which allele is positively (increases the risk) associated with the development of Alzheimer’s disease? What are the control groups in these studies? 2. The frequency of all three genotypes with Ɛ4 is 0.64 in AD patients and 0.31 in the control group in the United States; 0.47 in AD patients and 0.17 in the control group in Japan. Interpret these data. 3. L.W. has the genotype Ɛ4/Ɛ4. According to the Table 12-10, she has 30-50% genetic risk for Alzheimer’s disease, known as the late onset Alzheimer’s disease (LOAD) which typically develop after 60 years old. Is LOAD a complex disease? Present all your supporting arguments.
3. Researchers are investigating a newly discovered condition that greatly increases the likelihood of lung damage associated with the use of e-cigarettes. They found that 2% of their study population has the condition. The researchers believe they have found a useful marker locus for assessing the presence of the condition in individuals with unknown family history. They have found that, of those individuals with the condition, 99% have the marker allele M1. Of those without the condition, 99.8% have an alternative allele M2 at the marker locus. What is the probability that an individual has the condition if they have marker allele M1 and what do you conclude about the utility of the marker locus for indirect diagnosis?
1. A mutant allele in persons with familial hypercholesterolemia (FH) causes death due to a lack of liver receptors for LDL. Susceptible persons have half the normal number of receptors, while other individuals have the normal number of receptors. In a phenotypically normal couple, the man had a female 1st cousin (on his father’s side) who died from FH; the woman had a maternal uncle with FH. Using standard symbols, draw a pedigree of these couple’s families. Write the genotypes of each family member. Indicate your legend for symbols used.
Tristan da Cunha is a group of small islands in themiddle of the Atlantic Ocean. In 1814, a group of 15British colonists founded a settlement on these islands.In 1885, 15 of the 19 males on the island were lost ina shipwreck. In the late 1960s, four cases of retinitispigmentosa, which progressively leads to blindness,were found among the 240 descendants of these settlers remaining on the island. The frequency of retinitis pigmentosa in Britain is about 1 in 6000. Explainthe high incidence of this disease on Tristan daCunha relative to that seen in Britain.