5. The TYR gene encoding for tyrosinase from two individuals was analyzed. Ithas been found that one individual has a wild type TYR and the other one hasthe mutation. On the gel electrophoresis, the control unaffected and the mutanthave no difference in the mobility, i.e., no change in size. What type of mutationhad most likely occurred?

Mutations are sudden or random alteration or change in genetic material. Mutations can be large…

Answered: 5. The TYR gene encoding for tyrosinase…

Biochemistry

9th Edition

ISBN:9781319114671

Author:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Publisher:Lubert Stryer, Jeremy M. Berg, John L. Tymoczko, Gregory J. Gatto Jr.

Chapter1: Biochemistry: An Evolving Science

Section: Chapter Questions

Problem 1P

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14. DNA methyltransferase, an enzyme that methylates DNA, - ---- a. is expressed in a higher than normal amount in a tumor cell; its location is nuclear b.. is expressed in a higher than normal amount in a tumor cell; its location is cytoplasmic c. is expressed in a lower than normal amount in a tumor cell; its location is nuclear d. . is expressed in a lower than normal amount in a tumor cell; its location is cytoplasmic 15. In human cancers, a. Rb promoter is hypermethylated b. expression of CDK inhibitors is inhibited c. there is high level of cyclin D-CDK4/6 kinase activity, phosphorylating pRb d. a and b e. a, b and c 16. Cancer causing agents bring about their effect mainly in G1 phase of the cell cycle because a. the cell has just emerged from the quiescent G0 phase b. Gl phase is the longest c. All enzymes and cyclins are active in the G1 phase d. Cells respond to their extracellular growth signals during the Gl phase
7. Explain why a mutant Ras is an oncogene causing many human cancers
1.Your goal is to design a strategy to create thisfinal pDHFR plasmid for fusion protein expressionfrom the materials available:You have an empty pET21a expression vector and another vectorthat contains the fusion protein nucleotide sequence (pBluescript + GST-DHFR-His). (#) indicatesbp location ofenzyme cut: a.EcoRIonly, HindIII only, NotIonly, EcoRI and HindIII, EcoRI and NotI, or HindIII and NotI? b.Briefly explain the rationale for your selection. Please connect your rationale to the need for compatible ends without any further manipulation and required directionality of the DHFR fusion protein coding sequence relative to the T7 promoter that will drive its expression. c.What is the final size(kb)of your desired pDHFR plasmid ligation product based onyour design? d. Complete the chart providedto indicate thesize of all fragments(in bp)resultingfrom complete digestion of each plasmid givenyour strategy, andthe fragment(in kb)from each you would isolate for ligation.Please mind…
1. Determine the effect of the following mutations on the DNA sequence. In each case, the mutation is described after the sequence (REFER TO THE SUPPLEMENTAL DOCUMENT FOR GUIDANCE TO THIS QUESTION). Adenine nucleotide (A shown in red below) was inserted into the DNA sequence at the position indicated by the arrow). Write out the sequence of the mutated DNA and the protein made from it. What is the effect of this mutation on the protein? (For example, how will the mutation affect the length and sequence of the protein? What about the function of the protein?) A 3' TACATGG'TTGTGCTAATT 5'
5a. In Activity 1, you may have noticed that we mutagenized a haploid strain. Haploid strains are easier than diploid strains when screening for recessive loss-of-function mutations. Why?
4. Using the information in problem 3, make another plot showing how DX and DP (rates of production of cells and product) vary with D (on the same graph), covering the same range of dilution rates in problem 3. 5. Genetics & Gene Control A. Explain the difference between a DNA strand, a chromosome and a gene. B. Would a cell with a deletion or a point mutation be more likely to revert back to the original phenotype? Why? C. Define feedback repression. On a basic level, how does this work in a cell?
. All mutations that abolish function of the Rho termination protein in E. coli are conditional mutations;no cells with null mutations of the Rho-encoding genehave ever been isolated. What does this tell you aboutthe rho gene and its product?
8. In genetic screens of mutagenized yeast, temperature sensitive mutants defective in the secretory pathway (sec mutants) were identified. These mutants have helped scientists study the protein secretion pathway that is necessary/essential for life in eukaryotic cells. To identify sec mutants: mutagenized yeast cells were grown for 12 hours at low temperature, shifted to higher temperature for two hours, and then the population of cells were centrifuged in a density gradient. a. Mutagenized cells were first grown at the lower temperature and then shifted to the higher temperature. i. Why was the shift in temperature an important step of the experimental protocol? ii. Why would the experiment have been unsuccessful if the cells were grown exclusively at the higher temperature? b. After centrifugation, where would sec mutant cells be located compared to other cells in the population? Briefly explain why.
2. Sickle-cell anemia is a genetic disorder caused by the abnormal gene for hemoglobin S. A single substitution oc- curs in which glutamic acid is substituted for valine in the sixth position of the hemoglobin molecule. This change reduces hemoglobin's ability to carry oxygen. a. Discuss the process by which mutation occurs in base substitution. b. Biologists used gel electrophoresis to initially identify the mutant gene. Explain how gel electrophoresis could be applied to the identification of the gene mutation. Discuss the use of restriction enzymes. c. Hemoglobin S is transmitted as a simple Mendelian allele. Describe the outcome if a female who does not carry the abnormal allele mates with a male homozygous for the disease. Include a Punnett square and pheno- typic and genotypic ratios.
1. Suppose there was a mutation in the inducer of the lac operon, such that the inducer was unable to function. How would the lac operon be affected? Please explain your reasoning in 1-3 sentences.
1. Please tell me: What's a mutation in moleculer terms? 2. When a mutation deletes a base in genomic DNA, how does it affect the expression product production and reading frame? 3. How does induction control enzyme synthesis using lactose operon?
3. Bacteria are normally haploid organisms (1 copy of the genome), however it is possible to introduce a plasmid into the bacteria to create a pseudo-diploid situation. Here we have introduced a plasmid that carries the lac operon. Based on the following genotypes, predict the state of the beta-glactosidase enzyme (lac Z) in each of the following situations. I- = a mutation in the repressor protein that cannot bind to the operator Is = a mutation in the repressor protein that cannot be removed from the operator Oc = a mutation in the operator that cannot bind the repressor Z` = a mutation in beta-galactosidase that makes the enzyme non-functional Chromosome Lactose Present I, Z, O I, Z, O I. Z-.O I-,Z,O IS,Z-,Oc, Plasmid I, Z, O I, Z, O I, Z, Oc I,Z,O I,Z,O Yes No No Yes Yes Functional enzyme (yes/no) Phenotype (inducible constitutive, repressed constitutive regressed

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