24. 23andme is a direct to consumer genotyping company that uses a microarray to genotype peopleon 1 million known SNPS in the genome. A man who was adopted wants to know about his ancestry,and purchases a 23andme kit for himself. He finds that of each autosome pair, exactly one isclassified as 100% Sub-Saharan African, while the other is a mixture of various East Asian andEuropean components. He also finds that his X chromosome is 100% Sub-Saharan African. What canthis man confidently infer about his recent ancestry?a. His mother was of Sub-Saharan African descentb. His father was of Sub-Saharan African descentc. He has no Neanderthal ancestryd. He has no mutations relative to his parentse. 23andme mixed up two samples and he can't infer anything

Genetic analysis of one’s genome can give a lot of information about one’s ancestors. Since,…

Answered: 24. 23andme is a direct to consumer…

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter4: Pedigree Analysis In Human Genetics

Section: Chapter Questions

Problem 4QP: Pedigree Analysis Is a Basic Method in Human Genetic: What does OMIM stand for? What kinds of...

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A method for detecting methylated CpGs involvesthe use of a chemical called bisulfite, which convertscytosine to uracil but leaves methylated cytosine untouched. You want to know whether a particularCpG dinucleotide at one location in the genome ismethylated on one or both strands in a tissue sample.The genomic sequence containing this CpG is:5’...TCCATCGCTGCA…3’. You take genomicDNA from the sample tissue, treat it exhaustivelywith bisulfite, and then use flanking primers toPCR-amplify the region including this CpGdinucleotide. You then want to Sanger sequence(see Fig. 9.7) the amplified PCR product. a. After you treat genomic DNA with bisulfite, the twoDNA strands will melt into single strands. Why?b. Your answer to part (a) introduces a potential complication, because if you do not account for this result of bisulfite treatment, the PCR primers willnot amplify the DNA. What special considerationswould be necessary when you design your PCRprimers for this experiment? Could one pair…
Take a look at question 3 in More Genetic TIPS. Let’s suppose amale is heterozygous for two polymorphic sequence-tagged sites.STS-1 exists in two sizes: 211 bp and 289 bp. STS-2 also exists intwo sizes: 115 bp and 422 bp. A sample of sperm was collectedfrom this man, and individual sperm were placed into 30 separatetubes. Into each of the 30 tubes were added the primers that amplifySTS-1 and STS-2, and then the samples were subjected toPCR. The following results were obtained:
Pedigree Analysis Is a Basic Method in Human Genetic: What does OMIM stand for? What kinds of information are in this database?
Using figure 1 and the following background information answer the following questions. Identification of the genetic cause of hornlessness in cattle has been the subject of intensive genetic and genomic research, culminating in the nomination of two different candidate neomutations on cattle chromosome 1 that are predicted to have arisen 500-1,000 years ago: a complex allele of Friesian origin (PF), an 80,128 base pair (bp) duplication (1909352–1989480 bp), and a second, simple allele of Celtic origin (PC) corresponding to a duplication of 212 bp (chromosome 1 positions 1705834–1706045) in place of a 10-bp deletion (1706051–1706060)We report the use of genome editing using transcription activator-like effector nucleases (TALENs) to introgress the putative PC POLLED allele into the genome of bovine embryo fibroblasts to try and produce a genotype identical to what is achievable using natural mating, but without the attendant genetic drag and admixture. In our previous studies, we…
Susan’s grandfather was deaf, and passed down a hereditary form of deafness within Susan’s family as shown in Figure Q19–12.A. Is this mutation most likely to be dominant or recessive?B. Is it carried on an autosome or a sex chromosome? Why?C. A complete SNP analysis has been done for all of the 11 grandchildren (4 affected, and 7 unaffected). In comparing these 11 SNP results, how long a haplotype block would you expect to find around the critical gene? How might you detect it?
In an in situ hybridization experiment, a certain clonebound to only the X chromosome in a boy with no diseasesymptoms. However, in a boy with Duchenne musculardystrophy (X-linked recessive disease), it bound to theX chromosome and to an autosome. Explain. Could thisclone be useful in isolating the gene for Duchenne muscular dystrophy?
The DNA of every individual in the pedigree shown in image B (below) has been sequenced at the causative locus, all the non-shaded individuals are wild type apart from III.1 and III.6. III.1 and III.6 have both been proven to have the causative allele for the condition but they do not exhibit any of the phenotypic signs or symptoms. Based on this pedigree, what is the level of penetrance for the condition? Please give your answer as a percentage to one decimal place, give the number only, no percentage symbol. Given the information above I calculate the level of penetrance seen in image B to be "Blank" 1 percent.
The DNA of every individual in the pedigree shown in image B (below) has been sequenced at the causative locus, all the non- shaded individuals are wild type apart from III.1 and III.6. III.1 and III.6 have both been proven to have the causative allele for the condition but they do not exhibit any of the phenotypic signs or symptoms. Based on this pedigree, what is the level of penetrance for the condition? Please give your answer as a percentage to one decimal place, give the number only, no percentage symbol. ANSWER: Given the information above I calculate the level of penetrance seen in image B to be Blank 1 percent. A KEY Homozygous Homozygous Heterozygous Heterozygous Wild Type Male Female Male Female Male Note: Completely red symbol denotes an individual exhibiting the phenotype of interest CI || III IV V 1/4 1/2 1/2 1/2 1/2 Wild Type Female 1/4 1/2 Affected Known carrier Affected female Normal female Affected male Normal male D ●●●
Suppose, you want to detect the CAG repeat expansion within a particular gene (30 repeats in normal changes to 250 repeats in disease) in a certain disease. How will you diagnose this disease condition? Can you identify Y chromosome microdeletion (which involves the deletion of AZF locus) using conventional karyotyping? If not, then why? How will you diagnose a chromosomal translocation event? (Discuss any one of the processes)
To detect the CAG repeat expansion with a particular gene where 30 repeats in Normal changes to 250 repeats in a certain disease, how can we diagnose the condition. How To identify Y chromosome microdeletion ( which involves the deletion of AZF locus) using conventional karyotyping? If not then why. How will you diagnose a chromosomal translocation event?
What is a recombination unit in the context of the present analysis? How does it differ from the map units used in eukaryote genetics?
Generate a primer pair that is 6 base-pairs long to amplify the inversion, that will notamplify wildtype mini gene 5' ATGGTGCAAGATTAA 3' 3' TACCACGTTCTAATT 5'

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