DNA repair systems are responsible for maintaining genomic fidelity in normal cells despite the high frequency with which mutational events occur. What type of DNA mutation is generated by (a) UV radiation and (b) ionizing radiation? Describe the system responsible for repairing each of these types of mutations in mammalian cells. Postulate why a loss of function in one or more DNA repair systems typifies many cancers.
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DNA repair systems are responsible for maintaining genomic fidelity in normal cells despite the high frequency with which mutational events occur. What type of DNA mutation is generated by (a) UV radiation and (b) ionizing radiation? Describe the system responsible for repairing each of these types of mutations in mammalian cells. Postulate why a loss of function in one or more DNA repair systems typifies many cancers.
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- The figure below summarizes the results of an experiment evaluating the role of Ku80 gene DNA repair. The Ku80 Knock Out mice were generated by genetically deleting the Ku80 gene and the effects of ionizing radiation on lifespan were evaluated. Briefly explain why Ku80 deletion has the observed effects. What form of DNA damage is causing the reduced lifespan and which repair mechanism appears to be responsible for repair of these lesion in normal mice?(a) How does the duplication of individual genes occur? (b) individual that inherit a genetic condition known as xeroderma pigmentosum exhibit an extreme sensitivity to sunlight exposure and often develop skin cancer by the age of 10. What repair pathway is most likely disrupted as a result of such mutation? Explain why?(b): How many forms can naturally occurring DNA exist in? Explain how these forms are characterized. What properties of the functional groups determine the binding of DNA with anti-cancer agents? Explain.
- Because the degree of DNA methylation appears to be a relatively reliable genetic marker for some forms of cancer, researchers have explored the possibility of altering DNA methylation as a form of cancer therapy. Initial studies indicate that while hypomethylation suppresses the formation of some tumors, other tumors thrive. Why would one expect different cancers to respond differently to either hypomethylation or hypermethylation therapies?Point mutations in multiple tumor suppressor proteins have been linked to cancer. For example changes in the gene for adenomatous-polyposis-coli protein (APC gene) may result in colorectal cancer. Consider the following DNA sense strand. 3'-TAC CGG TTG TGA AGC TGA ATC-5' (i) (ii) (iii) (iv) Derive the mRNA molecule from the given DNA strand sequence above, paying attention to the polarity of the molecule. Write down the polypeptide chain sequence arising from the mRNA molecule of the question above, using the table of the genetic code (Table Q1 overleaf) and indicate the C- and the N-terminus of the peptide chain. Point mutations of a cytosine (C) often lead to the dysfunction of the APC protein. Write down all possible polypeptide chains that can result from all possible DNA mutations of cytosines, disregarding a mutation in the MET/START and STOP codons. I Specify which of the point mutations identified in (d) are redundant?Describe the role of mismatch repair (MMR) in DNA repair.Why do mutations in MMR proteins increase the risk ofhuman cancer?
- With age, somatic cells are thought to accumulate genomic "scars"as a result of the inaccurate repair of double-strand breaks by non homologous end-joining (NHEJ). Estimates based on the frequency of breaks in primary human fibroblasts suggest that by age 70 each human somatic cell may carry some 2000 NHEJ-induced mutations due to inaccurate repair. If these mutations were distributed randomly around the genome, how many genes would you expect to be affected? Would you expect cell function to be compromised? Why or why not? (Assume that 2% of the genome - 1.5% coding and 0.5% regulatory - is crucial information.)What common mutation occurs in many human cancers? Explain how it can have this effect.Elaborate repair mechanisms that prevent permanent mutations in DNA are associated with replication, yet no similar repair process is associated with transcription. Can you think of a reason for this difference between replication and transcription? (Hint: Think about the relative effects of a permanent mutation in a DNA molecule and one in an RNA molecule.)
- In the treatment of cancer, the basis for many types of chemotherapyand radiation therapy is that mutagens are more effective at killingdividing cells than nondividing cells. Explain why. What are possibleharmful side effects of chemotherapy and radiation therapy?Why do mutations in genes that encode DNA-repair enzymes often produce a predisposition to cancer?a. Some antibiotics, such as rifampin, interfere with the function of RNA polymerase. What biological process is rifampin disrupting? b. Some antibiotic-resistant M. tuberculosis bacteria have a single point mutation (CàT) in the rpoB gene that causes an amino acid change from serine (a polar amino acid) to leucine (a non-polar amino acid). What type of mutation is this? Do you expect this to have no effect, a small effect, or a large effect on the polypeptide produced? Explain your reasoning. c. The rpoB gene encodes a subunit of the bacterial RNA polymerase protein. The point mutation described in Question 2 causes a change in protein folding, which leads to the inability of the rifampin antibiotic to bind to the RNA polymerase. Which level(s) of protein structure is/are affected by this change?