Biology Now, 2e

Answers ■ A15

A1: There are so many genes on an individual chromosome that

deleting or adding an entire chromosome has massive effects on an

individual.

Q2: In which part of meiosis would you predict that chromosomal

abnormalities are produced? (Refer back to Chapter 6 if

ne c e s sa r y.)

A2: During metaphase, when paired chromosomes are separated.

Q3: Create a mnemonic to help remember the four kinds of

structural changes (for example, Doctors Improve Treatment

Da i ly).

A3: Answers will vary.

Figure 8.7

Q1: How do we know whether two chromosomes are homologous?

A1: If the chromosomes carry alleles of the same genes and align

during cell division, they are homologous.

Q2: In one sentence, explain how the terms “gene,” “locus,” and

“chromosome” are related.

A2: A gene is found at a particular location—a locus—on a

chromosome.

Q3: If hair color were determined by a single gene, what would be

an example of the gene’s alleles?

A3: B for brown hair, b for blonde hair.

Figure 8.9

Q1: Which of the children specified in this Punnett square

represents Felix? What is his genotype?

A1: Felix is the “affected son,” with genotype XaY.

Q2: Explain why Felix is neither homozygous nor heterozygous for

the WA S gene.

A2: The WA S gene is found on the X chromosome, and Felix

carries only one X chromosome because he is a male. Only with

two chromosomes are homozygous and heterozygous genotypes

possible.

Q3: Create a Punnett square to illustrate the offspring that could

result if Felix had children with a noncarrier woman. What is the

probability that a son would have WAS? What is the probability

that a daughter would be a carrier of WAS?

A3: A son would have a 0% probability of having WAS. A daughter

would have a 100% probability of being a carrier.

Figure 8.10

Q1: Which chromosome contains the gene for cystic fibrosis? For

Tay-Sachs disease? For sickle-cell disease?

A1: Cystic fibrosis: chromosome 7. Tay-Sachs disease:

chromosome 15. Sickle-cell disease: chromosome 11.

Q2: No known genetic disorders are encoded on the Y

chromosome. Why do you think this is?

A2: The Y chromosome has very few genes; further, any disorder

would always be expressed and therefore selected against.

Q3: In your own words, explain why most single-gene disorders

are recessive rather than dominant.

A3: Dominant, single-gene disorders experience heavier selection

than recessive disorders because they are always expressed (there

are no carriers).

Figure 8.12

Q1: Which of the children in this Punnett square represents Zoe?

What is her genotype?

A1: Zoe is the “affected child,” with genotype aa.

Q2: If Zoe’s parents had another child, what is the probability that

the child would have cystic fibrosis? That the child would be a CF

carrier?

A2: The child would have a 25% (¼) probability of having CF, and

a 50% (½) probability of being a carrier.

Q3: If Zoe is able to have a child of her own someday, and the other

parent is not a carrier of cystic fibrosis (he would likely be tested

before they chose to have children), what is the probability that the

child would have cystic fibrosis? That the child would be a carrier?

A3: The child would have a 0% probability of having CF, and a

100% probability of being a carrier.

Figure 8.13

Q1: What is the probability that a child with one parent who has

an autosomal dominant disorder will inherit the disease?

A1: 50%.

Q2: Why are there no carriers with a dominant genetic disorder?

A2: Anyone with the gene would express the disorder.

Q3: Because dominant genetic disorders are rare, it is extremely

rare for both parents to have the condition (genotype Aa). Draw

a Punnett square with two Aa parents. What proportion of the

offspring would have the disorder? What proportion would be

normal?

A3: 75% of the offspring would have the disorder; 25% would be

normal.

Figure 8.14

Q1: Which gene was missing or damaged in Felix’s case? From

what chromosome would a healthy copy be taken?

A1: The gene missing or damaged in Felix was the WA S gene.

A healthy copy of the gene would be taken from an X chromosome.

Q2: Why did Dr. Klein’s group first conduct gene therapy on mice

rather than on humans? What are the advantages and limitations

of this approach?

A2: In case of unforeseen problems or dangers, a human would not

be hurt during the early trials. The limitation is that mice are not

humans, so the results are not directly transferable.

Q3: If Felix has children of his own someday, will they run the

risk of inheriting his disorder, or has gene therapy removed that

possibility? Explain your reasoning.

A3: Gene therapy does not replace the damaged gene; it simply

enables a missing gene product to be made. Felix remains the same

genetically, so there will be a risk of his children inheriting the

disorder.