Proteins A,B,C, and D in the diagram are encoded by different genes and interact with each other. Imagine that a mutation in the gene for protein A changes one of the charged amino acid in the red circle area from positive to negative charge (blue arrow). this mutation results in a mutant phenotype. Assume a mutation in the gene for protein B occurs and the double mutants have a phenotype that is almost wild type. How would you best describe the mutation in gene B?
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- In McCune-Albright syndrome, fibrous connective tissue replaces bone, tan patches (café-au-lait spots) dot the skin, and hormone abnormalities cause early puberty and malfunction of the thyroid, pituitary, and adrenal glands. The phenotype is highly variable, and all patients are somatic mosaics for the mutation, which is in the gene GNAS1. Why is the condition seen only in mosaics?You are studying a mutation in mice, which acts dominantly. Mice that have only one copy of the allele carrying this mutation have a kinky tail phenotype. You identify the gene that the mutation affects and find that the codon that encodes the second amino acid in the predicted protein has been mutated to a stop codon. Would you characterize this mutation as a loss-of-function or a gain-of-function and what specific subtype (hypermorphic, antimorphic, etc. ) within these categories? Explain your reasoning.”Considering Figure 2-13, if you had a homozygous double mutant m3/m3 m5/m5, would you expect it to be mutant in phenotype? (Note: This line would have two mutant sites in the same coding sequence.)
- You have the following DNA coding sequence of a wild-type allele: 5’-ATG TTC CAG CTA GAT GAT ATG CTG GTA ATT GGG GAA CGC GCG CGG TAA-3’ For each of the following mutations: A. State whether the mutation is missense, nonsense, frameshift, or silent. B. Write the codon change that occurs for the missense, nonsense, and silent mutations (ex. GAA -- GAT). C. For frameshift mutations, write out the entire mutant sequence with each codon clearly indicated (if the frameshift creates a new stop codon, end the sequence at the new stop). Using the wild type DNA sequence above as a guide : Write the amino acid sequence of the mutants. Mutant 1: transition at nucleotide 23 Mutant 2: T --> G transversion at nucleotide 29 Mutant 3: an insertion of “A” after nucleotide 14 Mutant 4: transition at nucleotide 7 Mutant 5: An insertion of GG after nucleotide 40 Mutant 6: transition at nucleotide 15 Mutant 7: a deletion of nucleotide 25How do we know that the mutant Bar-eye phenotype in Drosophila is due to a duplicated gene region rather than to a change in the nucleotide sequence of a gene?Consider a single base insertion mutation between the 3rd and 4th codons in a natural gene that encodes a protein 100 amino acids long. Is it more likely that the protein produced by this mutant allele will be shorter or longer than 100 amino acids long?
- Familial retinoblastoma, a rare autosomal dominant defect, arose in a large family that had no prior history of the disease. Consider the following pedigree (the darkly colored symbols represent affected individuals): a. Circle the individual(s) in which the mutation most likely occurred. b. Is the person who is the source of the mutation affected by retinoblastoma? Justify your answer. c. Assuming that the mutant allele is fully penetrant, what is the chance that an affected individual will have an affected child?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 CF3Duchenne muscular dystrophy (DMD) is an X-linked recessive genetic disease caused by mutations in the gene that encodes dystrophin, a large protein that plays an important role in the development of normal muscle fibers. The Dystrophin gene is immense, spanning 2.5 million base pairs, and includes 79 exons and 78 introns. Many of the mutations that cause DMD produce premature stop codons, which bring protein synthesis to a halt, resulting in a greatly shortened and nonfunctional form of dystrophin. Some geneticists have proposed treating DMD patients by introducing small RNA molecules that cause the spliceosome to skip the exon containing the stop codon (A. Goyenvalle et al., 2004. Science 306:1796–1799). The introduction of the small RNAs will produce a protein that is somewhat shortened because an exon is skipped and some amino acids are missing, but it may still result in a protein that has some function. The small RNAs, antisense RNAs, used for exon skipping are complementary to…
- Duchenne muscular dystrophy (DMD) is an X-linked recessive genetic disease caused by mutations in the gene that encodes dystrophin, a large protein that plays an important role in the development of normal muscle fibers. The dystrophin gene is immense, spanning 2.5 million base pairs, and includes 79 exons and 78 introns. Many of the mutations that cause DMD produce premature stop codons, which bring protein synthesis to a halt, resulting in a greatly shortened and nonfunctionalform of dystrophin. Some geneticists have proposed treating DMD patients by causing the spliceosome to skip the exon containing the stop codon. Exon skipping would produce a protein that is somewhat shortened (because an exon is skipped and some amino acids are missing), but might still result in a protein that had some function (A. Goyenvalle et al. 2004. Science 306:1796–1799). Propose a possible mechanism to bring about exon skipping for the treatment of DMD.Sandhoff disease is due to a mutation in a gene that encodes a proteincalled hexosaminidase B. This disease has symptoms that aresimilar to those of Tay-Sachs disease. Weakness begins in the first 6 months of life. Individuals exhibit early blindness and progressive mental and motor deterioration. The family in the pedigree shown below has three members with Sandhoff disease, indicated with black symbols.You learned in Problem 21 in Chapter 7 that theneurodegenerative disease ALS can be caused by expansion of a hexanucleotide repeat region (5′-GGGGCC-3′)outside of the open reading frame (but within the firstintron) of the gene called C9ORF72. While a normalC9ORF72 allele has 2–23 copies of the hexanucleotiderepeat unit, dominant disease-causing alleles have hundreds or even thousands of copies. Researchers observed that the first intron of theC9ORF72 disease allele is transcribed not only fromthe normal template strand of DNA, but also from thenontemplate strand. Even more unusual, both types ofrepeat-region transcripts are translated in all six readingframes in an AUG-independent manner—a processcalled repeat-associated non-ATG translation, or RANtranslation. These discoveries led to the hypothesisthat the proteins made from the repeats mightcontribute to ALS.a. What polypeptides are made from the repeat-regiontranscripts?b. According to the RAN translation hypothesis, whyare…