The case of golden labs in which a mutation in a gene for the pigment transport protein results in a lack of pigment (the golden color) instead of the brown or black the results from the actual pigment genes, is an example of... Select one: a. multiple alleles b. epistasis c. genomic imprinting d. altered methylation

The case of golden labs in which a mutation in a gene for the pigment transport protein results in a lack of pigment (the golden color) instead of the brown or black the results from the actual pigment genes, is an example of... Select one: a. multiple alleles b. epistasis c. genomic imprinting d. altered methylation

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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Red–green color blindness in humans is due to an X-linked recessive gene. A woman whose father is color blind possesses one eye with normal color vision and one eye with color blindness. a. Propose an explanation for this woman’s vision pattern. Assume that no new mutations have spontaneously arisen. b. Would it be possible for a man to have one eye with normal color vision and one eye with color blindness?
A couple who are both heterozygous for an autosomal recessive mutation that is narrowly expressed and fully penetrant are planning on having three children. What is the probability that one their children will be normal (unaffected) and two children will have the recessive mutant phenotype? Show your work. Please answer this question using the Bayes’ Theorem
A man and a woman have a child with cystic fibrosis. Neither parent has cystic fibrosis. How could this happen? a) Both parents carry the cystic fibrosis allele, and each passed that allele to their child. b) The child had a spontaneous mutation on both copies of their CFTR alleles, leading to cystic fibrosis. c) One parent gave the child two copies of the cystic fibrosis CFTR allele. c) One parent gave the child a wild type CFTR allele, and the other parent gave them a cystic fibrosis CFTR gene.
A study of three generations in a family of a male colleague of the authors indicated that many of the man's blood relatives had died of cardiovascular accidents and coronary heart disease. Others died of other causes but were affected by high blood pressure. What are the implications of this information for the man in question? b. What information and help might a genetic counselor provide?
Suppose that you are studying the role of Protein B, which you believe plays a role in regulating PCD/Apoptosis in mice. You create two lines of mutant mice. One (bb) is homozygous for a loss-of-function allele of gene B. The other (Bb) is heterozygous, with one wild-type allele and one loss-of function allele. Initially you pay particular attention to two phenotypes of the resulting mice:(i) The morphology of their paws (see picture) (ii) The size of their brains & shape of their skulls. The bb mice have unusually large brains and unusual protrusions from their skulls. Based on these data, does it appear that Protein B, when present and active, favors or inhibits PCD/Apoptosis?Briefly explain your reasoning. The answer should address both the paw and brain/skull data.
Colorblindness and hemophilia are both X-linked traits in humans. Explain how a female who has a defective color vision gene on one X chromosome and a defective blood clotting gene causing hemophilia on the other X chromosome can be neither a hemophiliac nor colorblind? Please discuss the effect of Gene dosage compensation in your answer and in your answer describe the molecular process by which this occurs.
Consider a couple: a woman who is homozygous for a recessive mutation that causes X-linked colorblindness, and a man with full color vision (he does not carry a copy of the mutation). a) What is the probability that a son of this couple will be colorblind? b) What is the probability that a daughter of the couple will be colorblind?
What was the hypothesis of the X-linked cross conducted in the lab (between white-eyed female and re-eyed male) with the white mutation in Drosophila and written up in your lab report? A All female offspring will inherit red eyes from their mother because the mutation is X linked recessi B All female offspring will inherit white eyes from their mother because the mutation is X linked recessive. C All male offspring will inherit white eyes from their mother because the mutation is X linked recessive. D All male offspring will inherit red eyes from their mother because the mutation is X linked recessive. E All male offspring will inherit white eyes from their mother because the mutation is X linked dominant.
The coloration of calico cats is also the result of the inactivation of one of a female cat's sex chromosomes. In females, two X chromosomes are present in all cells but only one is active, the inactive one is called a BARR BODY. This is why the coat color is random, even among cloned calico cats that have identical genomes. Calico is a coat color found in cats, which is caused by a SEX-LINKED, CODOMINANT allele. KEY: B = Black R = Orange BR = Calico The following genotypes are possible; Female cats can be black XBXB, orange XRXR, or calico XBXR Male cats can be black XBY or orange XRY If you are a cat breeder, what type of parents should you choose to have the MOST number of calico kittens?
Usually, the mutant alleles studied in Drosophila experiments are recessive because: A. they are difficult to create. B. they are loss of function mutations. C. they do not survive as long as dominant alleles. D. they do not occur in wild-type flies.
How can you use this piece of information to help you explain to your friends what is the significance of mutations in the emergence of new genetic properties (alleles) that may result (or not) in new phenotypic characteristics? (Recall that not all SNPs affect phenotype.)
a. What is the Raly gene? What does it encode? How does it relate to the lethality of Ay? b. A heterozygous mouse AAy does not produce enough pigment and it is yellow. Homozygous individuals die during development, but AAy heterozygous do not. Why? You may use any graphic aid to explain this, if necessary. This means that you may use a Punnett square or a forking segregation diagram, or computations with fractions. c. Explain why there is a non-Mendelian 2:1 yellow/agouti phenotypic ratio in this cross.