Human Biology (MindTap Course List)
11th Edition
ISBN: 9781305112100
Author: Cecie Starr, Beverly McMillan
Publisher: Cengage Learning
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Textbook Question
Chapter 20, Problem 3RQ
What evidence indicates that a trait is coded by a dominant allele on an autosome?
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Chapter 20 Solutions
Human Biology (MindTap Course List)
Ch. 20 - Prob. 1RQCh. 20 - What is a carrier of a genetic trait?Ch. 20 - What evidence indicates that a trait is coded by a...Ch. 20 - Prob. 4RQCh. 20 - Explain what nondisjunction is, and give two...Ch. 20 - _______ segregate during ______. a. Homologues;...Ch. 20 - Prob. 2SQCh. 20 - Genes on the same chromosome tend to stay together...Ch. 20 - Prob. 4SQCh. 20 - A chromosomes structure can be altered by _______....
Ch. 20 - Nondisjunction can be caused by ________. a....Ch. 20 - A gamete affected by nondisjunction could have...Ch. 20 - Genetic disorders can be caused by __________. a....Ch. 20 - A person who is a carrier for a genetic trait...Ch. 20 - Prob. 10SQCh. 20 - If a couple has six boys, what is the probability...Ch. 20 - Human sex chromosomes are XX for females and XY...Ch. 20 - People with Down syndrome have an extra copy of...Ch. 20 - Prob. 4CTCh. 20 - Prob. 5CTCh. 20 - About 4 percent of people of Northern European...Ch. 20 - The following pedigree shows the pattern of...
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- What type of epigenetic mark is responsible for genomic imprinting?arrow_forwardWhat type of epigenetic change is responsible for genomic imprinting?arrow_forwardProvide a proof that a different phenotype can be produced from the same genotype. What are the possible causes for this different expression? How can the different gene interactions be differentiated from each other and from the Mendelian inheritance?arrow_forward
- a) Assume that colour is controlled by a single sex-influenced gene where green is expressed preferentially in males. Individuals I-1 and I-2 are homozygous for red and green respectively. Which individual/s in generation II will be red? b) If colour is a controlled by cytoplasmic DNA, which individual/s in generation II will be green?arrow_forwardWhat evidence suggests that differences in monozygotic twins may be caused by epigenetic effects?arrow_forwardWhy does a loss or an excess in genetic material lead to the expression of an abnormal phenotype?arrow_forward
- Assume that a gene controls the expression of a trait in which affected children occur only in families where one or both parents are also affected; children who are normal may have parents who are (1) both normal, (2) one normal and one affected, or (3) both affected. Is the gene for the affected condition completely dominant, co-dominant, incompletely dominant or recessive?arrow_forwardIn rats, the following genotypes of two independently assorting autosomal genes determine coat color: A_B_ (gray); A_bb (yellow); aaB_ (black); aabb (cream). A third gene pair on a separate autosome determines whether or not any color will be produced. The CC and Cc genotypes allow color according to the expression of the A and B alleles. However, the cc genotype results in albino rats regardless of the A and Balleles present. Determine the F1 phenotypic ratio of the following crosses: (a) AAbbCC x aaBBcc; (b) AAbbCC x aaBBcc; (c) AABBCC x AABbcc.arrow_forwardSuppose 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.arrow_forward
- Human females who are heterozygous for an X-linked recessive allele sometimes exhibit mild expression of the trait. However, such mild expression of X-linked traits in females who are heterozygous for Xlinked alleles is not seen in Drosophila. What might cause this difference in the expression of X-linked genes between human females and female Drosophila? (Hint: In Drosophila, dosage compensation is accomplished by doubling the activity of genes on the X chromosome of males.)arrow_forwardSuppose 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. Suggest one other aspect of mouse morphology or physiology that you might expect to be altered in the absence of Protein B. Briefly explain your reasoning. Also, based on the apparent effect of Protein B on the likelihood of PCD/Apoptosis, would you classify Protein B as the product of a proto-oncogene or of a tumor suppressor gene?arrow_forwardWhat is the degree of intensity with which a particular genotype is expressed in a phenotype?arrow_forward
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