ols Add-ons HelpLast edit was seconds ago| CalibriBIUA -三| 三12LI316. The characteristic of albinism (lack of pigment in skin and hair), can be caused by a singlegene. The following pedigree shows a family in which some people are affected byalbinism.345.7.III36.IV2.347.a. Using just the information on this pedigree, is albinism caused by a dominantII田%3D 12.34.6.洋洋課主美f. Are the children in generation IV likely to be carriers for the allele that causesalbinism?

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Description: ols Add-ons HelpLast edit was seconds ago| CalibriBIUA -三| 三12LI316. The characteristic of albinism (lack of pigment in skin and hair), can be caused by a singlegene. The following pedigree shows a family in which some people are affected byalbinism

Answered: Are the children in generation IV…

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Biology

Are the children in generation IV likely to be carriers for the allele that causes albinism?

Human Heredity: Principles and Issues (MindTap Course List)

11th Edition

ISBN:9781305251052

Author:Michael Cummings

Publisher:Michael Cummings

Chapter10: From Proteins To Phenotypes

Section: Chapter Questions

Problem 3CS: A couple was referred for genetic counseling because they wanted to know the chances of having a...

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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?
The pedigree pictured is of an extended family where a large percentage of family members develop colon cancer at an early age. In this family, individuals either get colon cancer before the age of 16, or they don’t get it at all. a) Based on the information you have been given, what evidence, if any, suggests an inherited contribution to the development of this disease? b) You take a medical history of all 33 people in the pedigree and discover that a large percentage drink a special coffee on a daily basis, while others do not. The individuals who do not drink coffee are I-1, II-2, II-4, II-9, III-7, III-13, IV-1, and IV-3. Could drinking this special coffee play a role in colon cancer? Explain.
A. Look at the pedigree, and DISREGARD individual II-8 for the moment. Is the pattern of inheritance of Unetan syndrome dominant or recessive? You may assume that the gene is FULLY-PENETRANT in this family. Please give two specific reasons that support your conclusion. B. Now, looking at BOTH the pedigree AND at the Southern blot, is this trait autosomal, X-linked, or Y-linked? Please give two specific reasons that support your conclusion. Once again, disregard II-8 for the moment. One of your two reasons must refer specifically to evidence present in the Southern blot. C. Define the gene alleles associated with Unetan syndrome. Your alleles MUST be consistent with the pattern of inheritance, AND your genetic notation must be consistent with that used throughout the course. Unetan syndrome allele: ________ Normal allele: ________
A rare blinding disease that has a relation to dengenerative factors is partially penetrant. In the following pedigrees for two families, the affected symptomatic individuals (black circles and squares) have been diagnosed with this disease due to the mutation in mitochondrial DNA m.14484T>C. If III.4 is homoplasmic for m.14484T>C in hair, blood, urine and other tissues examined. What will occur with IV.7 then?
Need help, please. What are the ratios for the progeny phenotype(s)?
PEDIGREE: Shaded individuals in the pedigree have a genetic disease. Individuals marrying into the family, that is individuals II–1, II–4 and II–6, have no history of the disease in their families.1. Determine the mode of inheritance ______________________________2. Give the genotypes of the following individuals
Tay-Sachs disease is a rare human disease in which toxic substances accumulate in nerve cells. The recessive allele responsible for the disease is inherited in a simple Mendelian manner. For unknown reasons, the allele is more common in populations of Ashkenazi Jews of eastern Europe. A woman is planning to marry her first cousin, but the couple discovers that their shared grandfather’s sister died in infancy of Tay-Sachs disease.a. Draw the relevant parts of the pedigree, and show all the genotypes as completely as possible. b. What is the probability that the cousins’ first child will have Tay-Sachs disease, assuming that all people who marry into the family are homozygous normal?
The accompanying pedigree is for a rare, but relativelymild, hereditary disorder of the skin.a. How is the disorder inherited? State reasons for youranswer.b. Give genotypes for as many individuals in thepedigree as possible. (Invent your own defined allelesymbols.)c. Consider the four unaffected children of parentsIII-4 and III-5. In all four-child progenies from parentsof these genotypes, what proportion is expected tocontain all unaffected children?(picture added)
Both karyotyping and G_banding techniques show normal chromosomal pattern, however pedigree analysis revealed abnormality of genetic origin, can you think of a reason that would explain the findings?
Ann's family has a history of cystic fibrosis, a recessive genetic disease. In the pedigree, family members who are afflicted with the disease are shown in red. Members who are unafflicted may or may not be carriers. Which of the given family members can be identified definitively as unafflicted carriers of cystic fibrosis?
PLEASE ANSWER THE FOLLOWING LETTERS: a,b,c, and d Examine the pedigree of the McGraw family shown below. Certain individuals in this family are affected by a brain condition that makes them more susceptible to vertigo. As a genetic counselor, you interview the family and draw DNA samples. You discover that the condition is caused by a mutation that changes the sequence 5’GCATTC3’ to 5’GAATTC3’ introducing an EcoRI cut site. You decide to amplify a 1200bp fragment from the DNA that spans this mutation and then digest it with EcoRI. You run the results on a gel next to a marker that shows bands at 2000bp, 1200bp, 900bp, 800bp, and 400bp. Some individuals from the pedigree are identified on the gel.