Problems and Questions for Chapter 16B Material

Problems and Questions for Chapter 16B Material - Name:...

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Name: Hellums, Jessica UTEID: JSH575 T/TH 2:30 Finklea Problems and Questions for Chapter 16B Material C33. During methyl-directed mismatch repair, why is it necessary to distinguish between the template strand and the newly made daughter strand? How is this accomplished? In methyl directed mismatch repair, the error occurs in the template strand but the mutation does not arise until the strand is replicated. Therefore, the mutation will arise in the newly made daughter strand after replication. For this reason, it is necessary for the repair mechanism to distinguish between the two strands so that it repairs the newly made daughter strand with the actual mutation. The mismatch is usually due to a tautomeric shift changing the way that a base will hydrogen bond. Because of this an incorrect base is incorporated during replication into the new daughter strand and must be corrected. When the original base in the template strand tautomerizes back to its typical conformation, it will not match with the newly incorporated base and therefore will form a bulge in the double stranded DNA. MutS can recognize this bulge and recruit MutH to the site. MutH is an endonuclease that can knick the strand at the bulge and also scan down the double stranded DNA to locate a methylated base. This methylated base will only be on the template strand because methylation of DNA occurs after replication and the daughter strand has not yet been methylated. At the location of the methylated base on the template strand, MutH will knick the daughter strand. Then an exonuclease can remove the bases between these two knicks and DNA polymerase can fill this gap and ligase can make the last phosphodiester bond. C38. What is the underlying genetic defect that causes xeroderma pigmentosum? How can the symptoms of this disease be explained by the genetic defect? People with XP cannot be allowed into sunlight because UV radiation causes pyrimidine dimers which require repair by specific enzymes, specifically uvrABC. People with XP have a mutation in one of the genes that encode the subunits of uvrABC (either uvrA, uvrB, or uvrC). A mutated gene causes one of the uvrABCs subunits to be nonfunctional and prohibits the enzyme from
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Problems and Questions for Chapter 16B Material - Name:...

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