I have provided all the information needed please help me out I am a bit confused Scientists suggest a major evolutionary shift may have occurred when some human populations in east Africa, near the equator, migrated inland and changed their diet.Instead of eating primarily marine creatures rich in vitamin D, they consumed pastured livestock and diminished their dietary intake of vitamin D. Considering ONLY therelationship between vitamin D and UV exposure, explain a possible effect of this lifestyle change over time on the frequency of light-skin in these populations. Cystic fibrosis (CF) is an autosomal recessive disorder. Several different individual point mutations in the CFTR gene cause cystic fibrosis. Two of the most common mutations (Aand B) are shown on the diagram below. The lines below the gene represent ASO (allele-specific oligonucleotide) probes and the regions of the gene to which they hybridize. The"wild type" probe hybridizes to the wild type allele and the "mutant" probe hybridizes to the mutant allele of this gene.ВCFTR geneProbe 1 wild typeProbe 3 wild typeProbe 2 mutantProbe 4 mutantFive people underwent ASO testing for cystic fibrosis using all four of the probes shown below. The results of this test are shown in the diagram.#1#2#3# 4#5Probe 1Probe 2Probe 3Probe 4

Human evolution is defined as "the process by which humans evolved on Earth from now-extinct apes."…

Scientists suggest a major evolutionary shift may have occurred when some human populations in east Africa, near the equator, migrated inland and changed their diet nstead of eating primarily marine creatures rich in vitamin D, they consumed pastured livestock and diminished their dietary intake of vitamin D. Considering ONLY the relationship between vitamin D and UV exposure, explain a possible effect of this lifestyle change over time on the frequency of light-skin in these populations.

Scientists suggest a major evolutionary shift may have occurred when some human populations in east Africa, near the equator, migrated inland and changed their diet nstead of eating primarily marine creatures rich in vitamin D, they consumed pastured livestock and diminished their dietary intake of vitamin D. Considering ONLY the relationship between vitamin D and UV exposure, explain a possible effect of this lifestyle change over time on the frequency of light-skin in these populations.

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter11: Genome Alterations: Mutation And Epigenetics

Section: Chapter Questions

Problem 16QP: Familial retinoblastoma, a rare autosomal dominant defect, arose in a large family that had no prior...

See similar textbooks

Similar questions

A RFLP is discovered that is linked to the gene for Duchenne’s muscular dystrophy (DMD). DMD is an X-linked, recessive trait. The RFLP is 2 map units from the gene for DMD. Consider the following pedigree and Southern blot using a probe that hybridizes to the RFLP. Which band/s is/are associated with DMD? What is the genotype for individuals 3 and 4? (Remember, this is an X linked disease, so use X’s and Y’s to denote). Individual 9 married a man who does NOT have muscular dystrophy, and she is pregnant. DMD is an X-linked trait. What is the probability for their child to have DMD? An amniocentesis is performed and it is determined that 9’s child in utero has only a 10 kb band that hybridizes to the same probe used above. What can you say about the child now?
You are attempting to genotype a series of cells at gene A through restriction enzyme digestion. You know that the wild type allele “A” has 2 restriction enzyme cutting sites, creating bands that are 100bp, 200bp, and 300bp. A mutation creating allele “a” removes one of these cutting sites, creating bands that are 100bp and 500bp. How many separate bands would you expect to see on a gel for a cell that is heterozygous Aa? please show work. thanks
There are two genetic disorders that result from mutation in imprinted genes: Prader-Willi syndrome, Angelman syndrome. Angelman syndrome results from deletion of UBE3A, which is a gene imprinted such that only the maternal copy is expressed. In the pedigree above, individual I-1 is heterozygous for a deletion of UBE3A and does not have Angelman syndrome. Individual I-2 is homozygous wild type for UBE3A. Which individuals in the pedigree are at risk for exhibiting Angelman syndrome, if any? (Who could potentially have the syndrome, based on what alleles it is possible for them to inherit and express?) Question 8 options: Only I-1 could have been at risk. If he does not have the syndrome, no one in the pedigree could. Only III-1 is at risk I-1, II-2, and III-1 are all at risk Only II-2 is at risk No one in the pedigree is at risk Both II-2 and III-1 are at…
The region of the normal hemoglobin gene used for genetic testing for sickle cell anemia contains a restriction site such that homozygous normal individuals show two DNA fragments. If a single nucleotide change in hemoglobin destroys that restriction site, then how many DNA fragments will be visible on a gel from individuals that are homozygous mutant? What about heterozygotes?
What is the difference of intragenic and intergenic regions? Please explain with drawing.
A hereditary disease is inherited as an autosomal recessive trait. The wild-type allele of the disease gene produces a mature mRNA that is 1250 nucleotides (nt) long. Molecular analysis shows that the mature mRNA consists of four exons that measure 400 nt (exon 1), 320 nt (exon 2), 230 nt (exon 3), and 300 nt (exon 4). A mother and father with two healthy children and two children with the disease have northern blot analysis performed. The results of the northern blot for each family member are shown below. a) Identify the genotype of each family member, using the size of mRNAs to indicate each allele. (For example, a person who is homozygous wild type is 1250/1250). b) Based on your analysis, what is the most likely molecular abnormality causing the disease allele?
Aliens with orang eye color allele (o) is recessive to the dominant black eye color allele (O). The locus of the orange gene from 10 pure breed orange eyes aliens and 10 pure breed black eyes aliens. You notice a difference in the DNA sequence linked to each allele of the orange gene and you decide to use it as a physical marker to follow recombination between this sequence linked to the orange gene. These sequences consist of short tandem repeat (STR) with two different number of repeats, each associated with one of the two orange gene alleles. a PCR test distinguishes the 10 repeat STR and the 6 repeat STR associated with the O and o alleles respectively. Using primers on each side of the STRs you can amplify by PCR this sequence and visualizing the size of the 10 repeat and 6 repeat STRs in an electrophoresis gel. You can follow the two STR sequences (10 and 6 repeats) linkage and recombination frequencies with the orange gene locus. The black eye aliens yield a PCR fragment that is…
A person with a rare genetic disease has a sample of her chromosomessubjected to in situ hybridization using a probe that is known to recognize band p11 on chromosome 7. Even though her chromosomes look cytologically normal, the probe does not bind to this person’s chromosomes. How would you explain these results? How would you use this information to positionally clone the gene that is related to this disease?
Prader-Willi syndrome is caused by a mutation in anautosomal maternally imprinted gene. Label the following statements as true or false, assuming that thetrait is 100% penetrant.a. Sons of affected males have a 50% chance of showing the syndrome.b. Daughters of affected males have a 50% chance ofshowing the syndrome.c. Sons of affected females have a 50% chance ofshowing the syndrome.d. Daughters of affected females have a 50% chanceof showing the syndrome.
There are two genetic disorders that result from mutation in imprinted genes: Prader-Willi syndrome and Angelman syndrome. Prader-Willi syndrome results from deletion of region 15q11-q13, which in healthy individuals is a region imprinted such that only the paternal copy is expressed. In the pedigree above, individual I-1 is heterozygous for a deletion of region 15q11-q13 and does not have Prader-Willi syndrome. Individuals I-2 and II-1 are both homozygous wild type for the region. Which individuals in the pedigree might have Prader-Willi syndrome? (Who could potentially have the syndrome, based on what alleles it is possible for them to inherit and express?) Question 9 options: Only II-2 could have Prader-Willi syndrome III-1 could have Prader-Willi syndrome in the presented pedigree; II-2 could only have had it if she were male Both II-2 and III-1 could have Prader-Willi syndrome II-2 could have…
You are using the restriction enzyme HAEIII to digest different samples of the taster gene isolated from cheek cells of different people and amplified by PCR. When viewing the bands on the electrophoresis gel, one would expect that a taster (homozygote) would have---------band(s), whereas a carrier (heterozygote) would show--------band(s), and a non-taster would show------band(s).
Cystic fibrosis can arise from a rare, short, in-frame deletion within the CFTR gene, whichcreates a recessive, disease-causing allele. Using this information, describe a PCRexperiment that could be undertaken to determine whether a healthy individual is acarrier of the cvstic-fibrosis mutation.