Polydactly is an autosomal dominant phenotype. In this pedigree, I-2 has one copy of the dominant allele and has polydactyly. Individuals l-2 and III-2 have extra thumbnails ontheir hands. Individuals Il-3, III-1 and III-4 have extra digits on both hands and feet, Il-4 has an extra digit on one hand.1-2Il-3II-4III-1 III-2 III-3 -4Is this an example of variable expressivity? Explain why or why not.

Name: Polydactly is an autosomal dominant phenotype. In this pedigree, I-2
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Description: Polydactly is an autosomal dominant phenotype. In this pedigree, I-2 has one copy of the dominant allele and has polydactyly. Individuals l-2 and III-2 have extra thumbnails ontheir hands. Individuals Il-3, III-1 and III-4 have extra digits on both

Variable expressivity occurs due to the similar genetic condition among different people which…

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Polydactly is an autosomal dominant phenotype. In this pedigree, I-2 has one copy of the dominant allele and has polydactyly. Individuals I-2 and Ill-2 have extra thumbnails or their hands. Individuals Il-3, III-1 and III-4 have extra digits on both hands and feet, Il-4 has an extra digit on one hand. 1-2 Il-3 Il-4 III-1 III-2 III-3 II-4 Is this an example of variable expressivity? Explain why or why not.

Polydactly is an autosomal dominant phenotype. In this pedigree, I-2 has one copy of the dominant allele and has polydactyly. Individuals I-2 and Ill-2 have extra thumbnails or their hands. Individuals Il-3, III-1 and III-4 have extra digits on both hands and feet, Il-4 has an extra digit on one hand. 1-2 Il-3 Il-4 III-1 III-2 III-3 II-4 Is this an example of variable expressivity? Explain why or why not.

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. Should the parents be concerned about the heterozygous condition as well as the homozygous mutant condition?
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?
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Adenike and her partner, Debare, are expecting their first child. Adenike is healthy as are her two sisters but her brother has PKU, a recessive disorder of the PAH gene. Genotypically he must be pah-/pah-. Neither of Adenike's parents has PKU but both of her grandmothers did. Debare is a carrier of Sickle Cell trait, which means he has one allele for wildtype hemoglobin (HbA) and one allele for Sickle Cell (HbS), making him HgA/HbS. More importantly, he has two alleles for Marfan Syndrome, a pleiotropic dominant disorder that can affect up to 30 different traits (M+/M+). No one in Debare's family has ever had PKU and no one in Adenike’s family has ever had Sickle Cell or Marfan Syndrome. They consult a genetics counselor over concern of the health of their baby. The genetics counselor collects the medical histories of three generations; their grandparents, their parents, and them. In her calculations, she produces a phenotypic key that indicates M = Marfan, Hb = sickle cell, and pah-…
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Adenike and her partner, Debare, are expecting their first child. Adenike is healthy as are her two sisters but her brother has PKU, a recessive disorder of the PAH gene. Genotypically he must be pah-/pah-. Neither of Adenike's parents has PKU but both of her grandmothers did. Debare is a carrier of Sickle Cell trait, which means he has one allele for wildtype hemoglobin (HbA) and one allele for Sickle Cell (HbS), making him HgA/HbS. More importantly, he has two alleles for Marfan Syndrome, a pleiotropic dominant disorder that can affect up to 30 different traits (M+/M+). No one in Debare's family has ever had PKU and no one in Adenike’s family has ever had Sickle Cell or Marfan Syndrome. They consult a genetics counselor over concern of the health of their baby. The genetics counselor collects the medical histories of three generations; their grandparents, their parents, and them. In her calculations, she produces a phenotypic key that indicates M = Marfan, Hb = sickle cell, and pah-…
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