Generation IGeneration IIGeneration III121 2 3 4O b.2O c.5O d.7O e. It is not possible to tell from the pedigree alone3142In the pedigree above (i.e., Figure F in the supplemental file), how many siblings does individual III-8 have?O a. 156по5 6 7 87 Generation IGeneration IIGeneration III12325672 3 45 6 7 8magine that the pedigree above (i.e., Figure F in the supplemental file) reflects individuals with and without a newly-discovered condition known as Netflixitis. Which individuals in Generation II have the condition?O a. Il-1, II-2, and II-4O b. 11-2, 11-4, 1I-6, and II-7O c. Il-1 and 11-5O d. Il-1, II-3, and II-5O e. Il-7

Name: Generation IGeneration IIGeneration III121 2 3 4O b.2O c.5O d.7O e. I
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Description: Generation IGeneration IIGeneration III121 2 3 4O b.2O c.5O d.7O e. It is not possible to tell from the pedigree alone3142In the pedigree above (i.e., Figure F in the supplemental file), how many siblings does individual III-8 have?O a. 156по5 6 7 8

Anyone who has at least one biological or adoptive parent in common is considered to be a sibling.…

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Generation I Generation II Generation III 1 2 1 2 3 4 3 1 4 2 5 опо 5 In the pedigree above (i.e., Figure F in the supplemental file), how many siblings does individual III-8 have? O a. 1 O b.2 O c.5 O d.7 Oe. It is not possible to tell from the pedigree alone 6 6 7 8 7

Generation I Generation II Generation III 1 2 1 2 3 4 3 1 4 2 5 опо 5 In the pedigree above (i.e., Figure F in the supplemental file), how many siblings does individual III-8 have? O a. 1 O b.2 O c.5 O d.7 Oe. It is not possible to tell from the pedigree alone 6 6 7 8 7

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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4. In this pedigree of another family with hemophilia A. If the woman Il-2 has a son, what is the chance that he is affected? II B. If the woman Il-2 has a daughter, what is the chance 1 2 3 4 III that she is affected? -1 C. If the woman Il-2 has 2 sons, what is the chance that neither will be affected? D. What are the chances that the child of II-4 and Il-5 will be affected?
а. What type of inheritance is shown in the pedigree? II 2 II 1 2 4 IV Identify the genotypes of the following individuals: III- 2 b. |-1 Il- 2 III-4 IV-1 + v Paragraph В I
Use the pedigree to answer the questions that follow. Make sure you put your answer in the correct blank. A) AB В 1 5 II A A AB B A AB A 3 5 6 7 8 II A A B 2 3 5 6 a) State the possible blood type(s) of individual I-4 b) State the possible blood type(s) of individual I-6 c) State the possible genotype(s) of individual Il-5 d) State the possible genotype(s) of individual II-6 e) Determine the percentage chance that couple Il-4 and Il-5 have another child that has type O blood 2.
Melanoma, 45 Colon cancer, 40 Sarcoma, 45 Breast Lung cancer, 53 cancer, 32 Stomach cancer, 50 Brain cancer, 18 Osteosarcoma, 3 Leukemia, 19 Rhabdomyosarcoma, 14 Answer the following subparts :- A. What do you notice in this pedigree as compared to Rb or BRCA1/2? B. Why do you think that so many cancer types are associated with inherited defects in p53? Please need detailed answer I want to learn please please I will upvote god promise|
6. Identify the mode of inheritance for the following pedigree. Provide the genotypes of indicated individuals. ? Genotypes: Il-1 IV-1 V-6 Il-2 IV-2 V-12 Il-3 IV-3 V- 14 III-1 IV-4 V-16 III-13 V- 1 V-19
1. The location of hemophilia C- factor XI is 4q35, where exactly is it? Describe.2. Referring to image of chromosome 16 provided, indicate the exact location of the geneslabeled a-k:
A genetic counsellor is working with a couple who have just had a child who has a debilitating autosomal recessive form of a disease termed epidemolysis bullosa (which causes severe external and internal skin fragility resulting in blistering etc). Neither parent has epidemolysis bullosa, nor does anyone in their families. What should the counsellor say to this couple? OA. "Because no one in either of your families has epidemolysis bullosa, you are not likely to have another baby with epidemolysis bullosa. You can safely have another child." OB. "Because you have had one child with epidemolysis bullosa, you must each carry the allele. Any child you have has a 50% chance of having the disease." OC. "Because you have had one child with epidemolysis bullosa, you must each carry the allele. Any child you have has a 25% chance of having the disease." OD. "Because you have had one child with epidemolysis bullosa, you must both carry the allele. However, since the chance of having an affected…
PART 3– Sex Linkage Hemophilia is a recessive sex-linked disorder in which an important clotting factor protein (Factor VIII) is not produced in a functional form. Queen Victoria was a carrier of the recessive Factor VIII allele, meaning she carried the allele but was asymptomatic. Recently, historians have discovered that she secretly had an affair with the Austrian Count Chocula, who, unbeknownst to her, was a hemophiliac. Naturally, the Royal Family fought to have this information suppressed, but it was revealed that they had many children together. 1. Using the correct allele notation, write the genotypes for Queen Victoria and Count Chocula. 2. In the Punnett Square below, show the cross between the Queen and the Count. P> PĮ
A couple was referred for genetic counseling because they wanted to know the chances of having a child with dwarfism. Both the man and the woman had achondroplasia (MIM 100800), the most common form of short-limbed dwarfism. The couple knew that this condition is inherited as an autosomal dominant trait, but they were unsure what kind of physical manifestations a child would have if it inherited both mutant alleles. They were each heterozygous for the FGFR3 (MIM 134934) allele that causes achondroplasia. Normally, the protein encoded by this gene interacts with growth factors outside the cell and receives signals that control growth and development. In achrodroplasia, a mutation alters the activity of the receptor, resulting in a characteristic form of dwarfism. Because both the normal and mutant forms of the FGFR3 protein act before birth, no treatment for achrondroplasia is available. The parents each carry one normal allele and one mutant allele of FGRF3, and they wanted information on their chances of having a homozygous child. The counsellor briefly reviewed the phenotypic features of individuals with achondroplasia. These include facial features (large head with prominent forehead; small, flat nasal bridge; and prominent jaw), very short stature, and shortening of the arms and legs. Physical examination and skeletal X-ray films are used to diagnose this condition. Final adult height is approximately 4 feet. Because achondroplasia is an autosomal dominant condition, a heterozygote has a 1-in-2, or 50%, chance of passing this trait to his or her offspring. However, about 75% of those with achondroplasia have parents of average size who do not carry the mutant allele. In these cases, achondroplasia is due to a new mutation. In the couple being counseled, each individual is heterozygous, and they are at risk for having a homozygous child with two copies of the mutated gene. Infants with homozygous achondroplasia are either stillborn or die shortly after birth. The counselor recommended prenatal diagnosis via ultrasounds at various stages of development. In addition, a DNA test is available to detect the homozygous condition prenatally. What if the couple wanted prenatal testing so that a normal fetus could be aborted?
A couple was referred for genetic counseling because they wanted to know the chances of having a child with dwarfism. Both the man and the woman had achondroplasia (MIM 100800), the most common form of short-limbed dwarfism. The couple knew that this condition is inherited as an autosomal dominant trait, but they were unsure what kind of physical manifestations a child would have if it inherited both mutant alleles. They were each heterozygous for the FGFR3 (MIM 134934) allele that causes achondroplasia. Normally, the protein encoded by this gene interacts with growth factors outside the cell and receives signals that control growth and development. In achrodroplasia, a mutation alters the activity of the receptor, resulting in a characteristic form of dwarfism. Because both the normal and mutant forms of the FGFR3 protein act before birth, no treatment for achrondroplasia is available. The parents each carry one normal allele and one mutant allele of FGRF3, and they wanted information on their chances of having a homozygous child. The counsellor briefly reviewed the phenotypic features of individuals with achondroplasia. These include facial features (large head with prominent forehead; small, flat nasal bridge; and prominent jaw), very short stature, and shortening of the arms and legs. Physical examination and skeletal X-ray films are used to diagnose this condition. Final adult height is approximately 4 feet. Because achondroplasia is an autosomal dominant condition, a heterozygote has a 1-in-2, or 50%, chance of passing this trait to his or her offspring. However, about 75% of those with achondroplasia have parents of average size who do not carry the mutant allele. In these cases, achondroplasia is due to a new mutation. In the couple being counseled, each individual is heterozygous, and they are at risk for having a homozygous child with two copies of the mutated gene. Infants with homozygous achondroplasia are either stillborn or die shortly after birth. The counselor recommended prenatal diagnosis via ultrasounds at various stages of development. In addition, a DNA test is available to detect the homozygous condition prenatally. What is the chance that this couple will have a child with two copies of the dominant mutant gene? What is the chance that the child will have normal height?
A couple was referred for genetic counseling because they wanted to know the chances of having a child with dwarfism. Both the man and the woman had achondroplasia (MIM 100800), the most common form of short-limbed dwarfism. The couple knew that this condition is inherited as an autosomal dominant trait, but they were unsure what kind of physical manifestations a child would have if it inherited both mutant alleles. They were each heterozygous for the FGFR3 (MIM 134934) allele that causes achondroplasia. Normally, the protein encoded by this gene interacts with growth factors outside the cell and receives signals that control growth and development. In achrodroplasia, a mutation alters the activity of the receptor, resulting in a characteristic form of dwarfism. Because both the normal and mutant forms of the FGFR3 protein act before birth, no treatment for achrondroplasia is available. The parents each carry one normal allele and one mutant allele of FGRF3, and they wanted information on their chances of having a homozygous child. The counsellor briefly reviewed the phenotypic features of individuals with achondroplasia. These include facial features (large head with prominent forehead; small, flat nasal bridge; and prominent jaw), very short stature, and shortening of the arms and legs. Physical examination and skeletal X-ray films are used to diagnose this condition. Final adult height is approximately 4 feet. Because achondroplasia is an autosomal dominant condition, a heterozygote has a 1-in-2, or 50%, chance of passing this trait to his or her offspring. However, about 75% of those with achondroplasia have parents of average size who do not carry the mutant allele. In these cases, achondroplasia is due to a new mutation. In the couple being counseled, each individual is heterozygous, and they are at risk for having a homozygous child with two copies of the mutated gene. Infants with homozygous achondroplasia are either stillborn or die shortly after birth. The counselor recommended prenatal diagnosis via ultrasounds at various stages of development. In addition, a DNA test is available to detect the homozygous condition prenatally. Should the parents be concerned about the heterozygous condition as well as the homozygous mutant condition?
Mike was referred for genetic counseling because he was concerned about his extensive family history of colon cancer. That family history was highly suggestive of hereditary nonpolyposis colon cancer (HNPCC). This predisposition is inherited as an autosomal dominant trait, and those who carry the mutant allele have a 75% chance of developing colon cancer by age 65. Mike was counseled about the inheritance of this condition, the associated cancers, and the possibility of genetic testing (on an affected family member). Mikes aunt elected to be tested for one of the genes that may be altered in this condition and discovered that she did have an altered MSH2 gene. Other family members are in the process of being tested for this mutation. Once a family member is tested for the mutant allele, is it hard for other family members to remain unaware of their own fate, even if they did not want this information? How could family dynamics help or hurt this situation?