4. Suppose that a parent Drosophila is e ca* e ca The gamete frequency is as follows: e'ca e'ca e ca е cа 31% 14% 16% 29% a. Circle the recombinant gametes. b. What is the map distance between the ebony and claret genes?
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- In Drosophila, the gene loci for curved wings and purple eyes are 20 centimorgans (map units) apart from each other on an autosomal chromosome. Wild-type flies were mated with double mutant flies with cv cv p p genotypes and curved wing/purple eye phenotypes. AlIl of the F1 flies had wild type phenotypes. The F, flies were crossed with double mutant flies with cv cv p'p genotypes and curved wing/purple eye phenotypes. What are the predicted percentages of flies in the F2 generation with wild type wings and eyes, curved wings and wild type eyes, wild type wings and purple eyes, and curved wings and purple eyes?You are given a Drosophila female that looks wild-type but is heterozygous for mutations intan body (t), miniature wings (m), and white eyes (w). You test cross this female with a tanbodied, miniature winged, and white-eyed homozygous mutant male, and you obtain thefollowing 1400 progeny: Phenotype : number+ + + : 608t m w : 516+ m w : 2t + + : 6+ m + : 39t + w : 46+ + w : 81t m + : 102 Calculate the distance between each pair t-m, m-w, and t-w only using the number ofrecombinants between them (i.e. ignoring the gene in the middle). Draw a linear map with thedistances between genes.Homozyogous wild type male Drosophila PPQQRRSSTTUUVV (all linked) are irradiated to induce the formation of chromosomal deletions and then mated with homozygous recessive females. In several of these matings a unique pattern of pseudodominance could be correlated with the loss of specific polytene chromosome bands, as shown in the table... Cross Chromosomal Bands Deleted Pattern of Pseudodominance PqRs TuV 1 2 3 4 5 5-6 1-2 3-5 6-8 1-3 PQRSTUV PqrSTUV PQRSTUV pQrSTUV In which chromosomal band is gene R located? A. 3 OB. 4 OC. 2 D.8 O E. none of these answers are correct
- The Drosophila gene Sex lethal (Sxl) is deserving of itsname. Certain alleles have no effect on XY animals butcause XX animals to die early in development. Other alleles have no effect on XX animals but cause XY animals to die early in development. Thus, some Sxl allelesare lethal to females, while others are lethal to males.a. Would you expect a null mutation in Sxl to causelethality in males or in females? b. Why do Sxl alleles of either type cause lethality ina specific sex?The gene transformer (tra) gets its name from sexualtransformation, as some tra alleles can change XXanimals into morphological males, while other traalleles can change XY animals into morphologicalfemales.c. Which of these sex transformations would becaused by null alleles of tra and which would becaused by constitutively active alleles of tra?d. In contrast with Sxl, null tra mutations do notcause lethality either in XX or in XY animals.However, the Sxl protein regulates the productionof the Tra protein. Why…I. Male Drosophila from a true-breeding wild-typestock were irradiated with X-rays and then mated withfemales from a true-breeding stock carrying the following recessive mutations on the X chromosome:yellow body (y), crossveinless wings (cv), cut wings(ct), singed bristles (sn), and miniature wings (m).These markers are known to map in the order:y - cv - ct - sn - mMost of the female progeny of this cross were phenotypically wild type, but one female exhibited ct and snphenotypes. When this exceptional ct sn female wasmated with a male from the true-breeding wild-typestock, twice as many females as males appearedamong the progeny.a. What is the nature of the X-ray-induced mutationpresent in the exceptional female?b. Draw the X chromosomes present in the exceptional ct sn female as they would appear duringpairing in meiosis.c. What phenotypic classes would you expect to seeamong the progeny produced by mating the exceptional ct sn female with a normal male from a truebreeding wild-type…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?
- 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?Another gene in Drosophila determines wing length. The dominant wild-type allele of this gene produces long wings; a recessive allele produces vestigial (short) wings. A female that is true- breeding for red eyes and long wings is mated with a male that has purple eyes and vestigial wings. F1 females are then crossed with purple-eyed, vestigial-winged males. From this second cross, a total of 600 offspring are obtained with the following combinations of traits: 252 with red eyes and long wings 276 with purple eyes and vestigial wings 42 with red eyes and vestigial wings 30 with purple eyes and long wings Are the genes linked, unlinked, or sex-linked? If they are linked, how many map units separate them on the chromosome?
- Almost all calico cats (one is pictured in FIGURE 10.7B) are female. Why? B When this calico cat was an embryo, one of the two X chromosomes was inactivated in each of her cells. The descendants of the cells formed her adult body, which is a mosaic for expression of X chromosome genes. Black fur arises in patches where genes on the X chromosome inherited from one parent are expressed; orange fur arises in patches where genes on the X chromosome inherited from the other parent are expressed. FIGURE 10.7 Animated X chromosome inactivation.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?Considering the following chromosome which is represented as a series of genes on each arm separated by the centromere. Describe the type of mutation required to produce each of the mutant chromosomes below. ABCDEFG*HIJKLMN