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- 32. A 23-year-old man comes to the physician because of a 1-month history of weakness and muscle pain after vigorous exercise. His mother, sister, and grandmother have a similar condition; however, his father's sister and her children are unaffected. A muscle biopsy specimen shows ragged red fibers. This condition most likely results from a mutation in a gene located in which of the following labeled structures in the photomicrograph? 00 O O A) B) E) B A E D C AR4e. 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' * promoter1. 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.)
- 1. Huntington's disease (HD) is an autosomal dominant, 12 neurodegenerative disorder caused by a pathological expansion of CAG repeats in the gene encoding for a protein called huntingtin. CAG codes for glutamine, and huntingtin protein containing > 42 ex- tra C-terminal Gln residues causes pathology. There has been sig- nificant evidence that energy production is impaired in HD, but the origin of the hypometabolism, i.e., glycolysis vs. oxidative phosphor- ylation, was not established until fairly recently. wild-type 10 mutant 8 2 The diagram on the right compares in the upper diagram the total ATP production generated in cultured (wt) STHDHQ7/Q7 and mu- tant STHDHQ111/Q111 striatal neuronal progenitor cells. Within the standard error of the measurements, the ATP production proved un- expectedly to be equivalent from both types of cells. To probe the two different sources of ATP production in the cells, the investigators carried out similar experiments with permeabilized cells…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’ 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).1A.If transcription factor G is downstream of EGFR and upregulates gene H, what happens to H if Grb2 has an ER signal sequence? 1B. If transcription factor A is phosphorylated by Akt and upregulates gene B, what happens to gene B if a PI3K inhibitor is added? Choices are: A. No expression of the gene B. Upregulation even in the absence of stimulation/ EGF C. Upregulation but only in the presence of cytokine/ EGF
- 1. Describe which enzymes are required for lactose and tryptophan metabolism in bacteria when lactose and tryptophan, respectively, are (a) present and (b) absent. 2. Contrast positive versus negative regulation of gene expression. Describe the role of the repressor in an inducible system and in a repressible system./20. In class, we discussed diffferent types of genetic change that can cause a normal gene (proto- oncogene) to become a cancer-causing gene (oncogene), Which of the following would not be a cause? A) translocation or transposition (movement of DNA within the same genome) B) gene ampliffication (increased number of copies of a given gene) C) epigenetic change D) point mutation that changes the gene's product E) loss of telomeres during DNA replication ancer?1. The following image shows a mechanism in which gene expression activity is regulated by ligand. Arg RS-2 Teu Met RBS Ligand RBS hidden a. What is this kind of regulatory machnism called? b. Does it involve transcription or translation? c. What happens in the presence of the ligand? d. What happens in the absence of theligand? e. What do you think the genes that are regulated here - metabolic (breakdown) or anabolic (buildup) for the ligand? Explain
- 13. Two transcription factors, A and B, are required to bind an enhancer, E, in order for Gene X to be transcribed (see diagram) 00 Gene X Let a and b represent recessive amorphic alleles of the transcription factors and E represent a deletion of the enhancer. Assuming Gene X IS haplosufficient, what phenotype will the following individuals have? Individual 1: Ala B/b E/E Individual 2: A/A B/B E/E- a. Individual 1: Wildtype; Individual 2: Wildtype b. Individual 1: Mutant; Individual 2: Wildtype c. Individual 1: Wildtype; Individual 2: Mutant d. Individual 1: Mutant; Individual 2: Mutant3). Consider the four mutations (i-iv) described below: i. One of the mutations causing cystic fibrosis in humans is a deletion of three nucleotides that eliminates a phenylalanine at position 508 of the CFTR protein (D508). Normally, CFTR protein is localized to the plasma membrane, where it functions as a chloride ion channel. D508 CFTR is misfolded and all of it is degraded without ever reaching the cell surface. ii. The yeast transcription factor Gal4p contains a DNA-binding domain and a transcriptional activation domain. An allele with a deletion the gene portion encoding the activation domain encodes a truncated Gal4p containing only the DNA-binding domain. It binds to Gal4p target genes at appropriate binding sites in their upstream regulatory regions, but does not activate their transcription. In cells with both wild type and mutant forms of Gal4p, the truncated Gal4p binds more efficiently to target DNA sequences than wild type. iii. Mutations in the acid maltase gene in…1. (a) Tryptophan-repressor complex binds to operator Gene is switched ON Gene is switched OFF Does NOT affect the gene expression (b) Operator is not bound with the repressor Gene is switched ON Gene is switched OFF Does NOT affect the gene expression