The Figueroa family has a genetically inherited trait called ocular albinism-lack of pigment in the eye-which is caused by a 516-bp deletion in an exon of a single gene. DNA for this gene was amplified from each member of the family and run on the gel shown below. The thickness of the band indicates relative amount of DNA. Use the pedigree and the gel to determine the most likely mode of inheritance for this disease. Becky Ben Jasper Lyla Sam Autosomal dominant Cannot be determined Autosomal recessive X-linked dominant X-linked recessive Becky Jasper Lyla Ben Sam

The Figueroa family has a genetically inherited trait called ocular albinism-lack of pigment in the eye-which is caused by a 516-bp deletion in an exon of a single gene. DNA for this gene was amplified from each member of the family and run on the gel shown below. The thickness of the band indicates relative amount of DNA. Use the pedigree and the gel to determine the most likely mode of inheritance for this disease. Becky Ben Jasper Lyla Sam Autosomal dominant Cannot be determined Autosomal recessive X-linked dominant X-linked recessive Becky Jasper Lyla Ben Sam

Name: The Figueroa family has a genetically inherited trait called ocular a
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Description: The Figueroa family has a genetically inherited trait called ocular albinism-lack of pigment in the eye-which is caused by a 516-bp deletion in an exon of a single gene. DNA forthis gene was amplified from each member of the family and run on the ge

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...

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If you had the ability to do gene editing with ONE gene for the betterment of human kind, which one would you choose, and why? Assume you could either change an abnormal allele associated with a disease, such as the cystin gene associated with Cystic Fibrosis to its normal wild type, or add a pre-existing human allele to a genome.
Pedigree Analysis Is a Basic Method in Human Genetics Using the pedigree provided, answer the following questions. a. Is the proband male or female? b. Is the grandfather of the proband affected? c. How many siblings does the proband have, and where is he or she in the birth order?
Which members of the pedigree could have been carriers, and which might have been the source of the mutation?
Pedigree Analysis Is a Basic Method in Human Genetic: What does OMIM stand for? What kinds of information are in this database?
The Figueroa family has a genetically inherited trait called ocular albinism—lack of pigment in the eye—which is caused by a 516-bp deletion in an exon of a single gene. DNA for this gene was amplified from each member of the family and run on the gel shown below. The thickness of the band indicates the relative amount of DNA. Use the pedigree and the gel to determine the most likely mode of inheritance for this disease. a) x-linked dominant b)x-linked recessive c)autosomal dominant d) autosomal recessive e) cant be determined
n the pedigree below, the letters in each symbol represent the genotype of the individual for a specific gene. Use the pedigree to answer the following questions about the tamarin family.
John Doe has two possible fathers. The DNA fragment sizes of John Doe, John Doe's mother, a possible fathers are as follows: John Doe's mother - 850 bp and 400 bp John Doe - 680 bp and 400 bp Possible father 1 - 680 bp and 500 bp Possible father 11 - 680 bp and 280 bp Which, If either of the two men could be John Doe’s father and why? A. both of the two men, because they and John Doe all have a 680 bp sized DNA fragment B. possible father II because both he and John Doe have a 680 bp sized DNA fragment C. possible father I because both he and John Doe have a 680 bp sized DNA fragment D. neither man, because neither has a 400 bp sized DNA fragment
Using the figure and the following background information answer the following questions about the figure Background: 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…
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…
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…
In a study of a muscle disorder, several affected families exhibited vision problems, muscle weakness, and deafness (M. Zeviani et al. 1990. American Journal of Human Genetics 47:904–914). Analysis of the mtDNA from affected members of these families revealed that large numbers of their mtDNA molecules possessed deletions of varying lengths. Different members of the same family and even different mitochondria from the same person possessed deletions of different sizes, so the underlying defect appeared to be a tendency for the mtDNA of affected persons to have deletions. A pedigree of one of the families studied is shown below. The researchers concluded that this disorder is inherited as an autosomal dominant trait, and they mapped the diseasecausing gene to a position on chromosome 10 in the nucleus. Q. What characteristics of the pedigree rule out inheritance of a trait encoded by a gene in the mtDNA as the cause of this disorder?
In a study of a muscle disorder, several affected families exhibited vision problems, muscle weakness, and deafness (M. Zeviani et al. 1990. American Journal of Human Genetics 47:904–914). Analysis of the mtDNA from affected members of these families revealed that large numbers of their mtDNA molecules possessed deletions of varying lengths. Different members of the same family and even different mitochondria from the same person possessed deletions of different sizes, so the underlying defect appeared to be a tendency for the mtDNA of affected persons to have deletions. A pedigree of one of the families studied is shown below. The researchers concluded that this disorder is inherited as an autosomal dominant trait, and they mapped the diseasecausing gene to a position on chromosome 10 in the nucleus. Q. Explain how a mutation in a nuclear gene might lead to deletions in mtDNA.