5. Deficiency of gene 5 expression leads to duplex kidney phenotype. Determine genotype(s) of mice From this cross predicted to have this phenotype. Explain your reasoning. X P M P Gene 5 Gene 5 Normal kidney Wildtype P M P Gene 5 Gene 5 Duplex kidney Gene 5 deficient
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- 1. A monogenic disease is a disease caused by a mutation in a single gene. For instance, sickle-cell anemia is caused by a mutation in the HBB gene, which codes for the B- globin chain of hemoglobin. The beginning of HBB is shown here: 5'-ATGGTGCACCTGACTCCTGAGGAGAAGTCTGCCGTTACT...-3' A. Translate this HBB sequence into an amino acid sequence. B. In terms of amino acids, what is the result of the sickle cell mutation, wherein the bolded red A is changed to a T? This single mutation causes hemoglobin to aggregate, causing red blood cells to deform into a sickle-like shape rather than the normal “biconcave disk" shape. C. What would happen if the bolded blue A were mutated to at T? (This is hypothetical; it's not a mutation found in sickle-cell disease.)4e. You also study the expression of 3 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'...TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3' 3' ...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5' * promoter4e. You also study the expression of 3 different mutants for this gene. For each mutant answer the following: Does this mutation change the sequence of the protein produced? Why or why not? If it does change the sequence of protein be sure to write out the new sequence. If it does not change the protein sequence, what effect (if any) would you expect it to have on expression of the gene? 1 20 ORI 40 60 5'..TTCGAGCTCTCGTCGTCGAGATACGCGATGATATTACTGGTAATATGGGGATGCACTATC...3’ 3'...AAGCTCGAGAGCAGCAGCTCTATGCGCTACTATAATGACCATTATACCCCTACGTGATAG...5’ promoter i. Mutant A has a single base pair substitution with the T/A being replaced with C/G base pair at position 35 (position denoted by the * in the sequence above). ii. Mutant B has a 2 G/C pairs inserted between position 19 and 20 (position denoted by the ^ in the sequence above).
- 2. For a fictional human tissue, it is hypothesised that cancer stem cells have the following expression pattern of cell surface markers (CD44+/CD24+/ESA+). Flow cytometry was used to isolate this population of cells. COMM CD24 ESA 1% Tumour volume (cm³) a) In the flow cytometry experiment, explain how to determine what percentage of the total cell population are the putative cancer stem cells. Also, briefly describe two controls that should be included in the experimental design. (30%) 3.01 2.5- +602 In a follow-up experiment, sorted and unsorted cells were injected subcutaneously into immunodeficient mice. The following plot depicts the results from the experiment. 2.0- 1.5- 1.0- CD24 0.5- ESA 37% • Unsorted CD44+/CD24+/ESA+ CD44+/CD24-/ESA- Time (weeks) 10 12AaBbCcDdE AaBbCcDc AaBbC Normal No Spacing Heading 1 Head Activity 1. 3. Based on the following data which of the following would be considered: a. Recessive? b. Dominant? C. A weak loss-of-function mutation? d. A null mutation? e. A haploinsufficiency ? Data - Gene "B" is required for formation of body segments. A wild type fly had 3 body segments. BB (Homozygous dominant) Wild Type Bb (Heterozygous) bb (Homozygous recessive) Lacks all body segments 1 body segment Mutant 1 Wild Type Mutant 2 Wild Type 2 body segments Mutant 3 Wild Type Wild Type 2 body segments Activity 4 tv Ps X W 000 DII DD II. Mutations in an autosomal gene in humans cause aform of hemophilia called von Willebrand disease(vWD). This gene specifies a blood plasma proteincleverly called von Willebrand factor (vWF). vWFstabilizes factor VIII, a blood plasma protein specified by the wild-type hemophilia A gene. Factor VIIIis needed to form blood clots. Thus, factor VIII is rapidly destroyed in the absence of vWF.Which of the following might successfully be employed in the treatment of bleeding episodes in hemophiliac patients? Would the treatments workimmediately or only after some delay needed forprotein synthesis? Would the treatments have only ashort-term or a prolonged effect? Assume that allmutations are null (that is, the mutations result in thecomplete absence of the protein encoded by the gene)and that the plasma is cell-free.a. transfusion of plasma from normal blood into avWD patientb. transfusion of plasma from a vWD patient into adifferent vWD patientc. transfusion of plasma from a hemophilia A…
- 3 Other (mutant) Gene: Clot, Please use "cl" abbreviation C A homozygous wt organism has been crossed to a homozygous mutant for your gene and for withered wings (whd). The resulting heterozygote is test-crossed. Predict the test cross results.1. If there were only two alleles of TAS2R38 (AVI and PAV) in the human population, what are the possible allelic combinations in diploid cells? 2. For the sake of simplicity, assume that only the amino acids Pro, Ala and Val make up the functioning active site pocket within the taste receptor TAS2R38. Using your knowledge of amino acid properties, describe the environment of the active site. Is it surprising that changing these amino acids to Ala, Val and Iso, respectively, inhibits the receptor from binding PTC?The cystic fibrosis gene encodes a chloride channel protein necessary for normal cellular functions. Let us assume that if at least 5% normal channels are present, the affected individual has mild symptoms of cystic fibrosis. Having less than 5% normal channels produces severe symptoms. At least 50% of the channels must be expressed for the individual to be phenotypically normal. This gene has various mutant recessive alleles: Predict the percent of functional channels and severity of symptoms for the following genotypes: a. heterozygous for CF100 b. homozygous for CF100 c. heterozygous, with one copy of CF100 and one of CF3 d. heterozygous, with one copy of CF1 and one copy of CF3
- The ABO blood groups in humans are expressed as the IAlB, and IAalleles. The allele encodes the A blood group antigen, lBencodes B, and i encodes O. Both A and B are dominant to O. If a heterozygous blood type A parent (IAi) and a heterozygous blood type B parent (IBi) mate, one quarter of their offspring will have AB blood type (IAIB) in which both antigens are expressed equally. Therefore, ABO blood groups are an example of: multiple alleles and incomplete dominance codominance and incomplete dominance incomplete dominance only multiple alleles and codominanceI. The retinoic acid receptor (RAR) is a transcription factor that is similar to steroid hormone receptors. Thesubstance (ligand) that binds to this receptor is retinoicacid. One of the genes whose transcription is activatedby retinoic acid binding to the receptor is myoD. Thediagram that follows shows a schematic view of theRAR proteins produced by genes into which one oftwo different 12-base double-stranded oligonucleotides had been inserted in the ORF. The insertion site(a–m) associated with each mutant protein is indicatedwith the appropriate letter on the polypeptide map.For constructs encoding proteins a–e, oligonucleotide 1(5′ TTAATTAATTAA 3′ read off either strand) wasinserted into the RAR gene. For constructs encoding proteins f–m, oligonucleotide 2 (5′ CCGGCCGGCCGG 3′)was inserted into the gene.NH2 f g h i j k l m COOHa b c d eThe wild-type RAR protein can both bind DNA and activate transcription weakly in the absence of retinoic acid(RA) and strongly in RA’s presence. Each…1. The location of hemophilia C- factor XI is 4q35, where exactly is it? Describe.2. Referring to image of chromosome 16 provided, indicate the exact location of the geneslabeled a-k:
