You start your experiments with the eyeless mutation on chromosome IV. You cross the reciprocal translocation strain to the eyeless pure line to generate F, flies that are both translocation heterozygotes and Ee heterozygotes. You decide to testcross F, males and females in two separate experiments to take advantage of the fact that crossing over does not occur in male Drosophila. F, males x pure eyeless females (Note: There is no crossing over F, females x pure eyeless males (Note: Crossing over in the F, males.) Cross may occur in the F, females.) 4 eyeless, fully fertile 4 wild-type, semi-sterile 4 eyeless, semi-sterile 4 wild-type, fully fertile % eyeless, fully fertile 4 wild-type, semi-sterile 4 eyeless, semi-sterile 4 wild-type, fully fertile F, Progeny What can you conclude from these results? Select the two correct statements. > View Available Hint(s) O The F2 progeny in both experiments contain recombinants. O The F2 progeny contain recombinants only when F, females are testcrossed. None of the F2 progeny classes require crossing over. O Chromosome IV is one of the chromosomes involved in the reciprocal balanced translocation.

In Drosophila, two genes, one for body color and one for eye color, are carried on the same chromosome. The wild-type gray body color is dominant to black body color, and wild-type red eyes are dominant to purple eyes. You make a cross between a fly with gray body and red eyes and a fly with black body and purple eyes. Among the offspring, about half have gray bodies and red eyes and half have black bodies and purple eyes. A small percentage have: (a) black bodies and red eyes; or (b) gray bodies and purple eyes. What alleles are carried together on the chromosomes in each of the flies used in the cross? What alleles are carried together on the chromosomes of the F1 flies with black bodies and red eyes, and those with gray bodies and purple eyes?

A colleague e-mails you saying that she has identified an interesting chromosome variation at 21q13. In discussing this discovery with a friend who is not a cytogeneticist, explain how you would describe this location, defining each term in the chromosome address 21q13.

A geneticist discovers that a girl with Down syndrome has a Robertsonian translocation involving chromosomes 14 and 21. If she has an older brother who is phenotypically normal, what are the chances that he is a translocation carrier?

Equalizing the Expression of X Chromosome Genes in Males and Females Individuals with an XXY genotype are sterile males. If one X is inactivated early in embryogenesis, the genotype of the individual effectively becomes XY. Why will this individual not develop as a normal male?

People with Down syndrome have an extra copy of chromosome 21, for a total of 47 chromosomes. However, in a few cases of Down syndrome, 46 chromosomes are present. This total includes two normal-looking chromosomes 21, one normal chromosome 14, and a longer-than-normal chromosome 14. Interpret this observation. How can these individuals have 46 chromosomes?

The gene controlling ABO blood type and the gene underlying nail-patella syndrome are said to show linkage. What does that mean in terms of their relative locations in the genome? What does it mean in terms of how the two traits are inherited with respect to each other?

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?

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 if the couple wanted prenatal testing so that a normal fetus could be aborted?