. It is thought that the signal for eukaryotic mismatch repair, for iden-tifying the strand to be repaired, could be nicks in the DNA to berepaired. If so, would you expect the nicked strand or the intactstrand to be the strand to be repaired? Briefly explain your answer.

DNA : it is the molecule that contains the genetic code of organisms. DNA is in each cell in the…

Answered: . It is thought that the signal for…

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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Describe how helicase, topoisomerase, and single-strand binding protein are important for the unwinding of the DNA double helix.
DNA polymerase occasionally incorporates the wrong nucleotide during DNA replication. If left unrepaired, the base-pair mismatch that results will lead to mutation in the next replication. As part of a template strand, the incorporated wrong base will direct the incorporation of a base complementary to itself, so the bases on both strands of the DNA at that position will now be different from what they were before the mismatch event. The MER-minus strain of yeast does not have a functional mismatch excision repair system, but it has normal base excision repair and nucleotide excision repair systems. Which of the following statements is correct about differences in the mutation spectrum between MER-minus and wildtype yeast? More than one answer is correct. Options: More point mutations will arise in MER-minus yeast. Fewer point mutations will arise in MER-minus yeast as compared with wildtype. Of the total point mutations that…
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Describe three major differences between leading and lagging strand synthesis. What feature of DNA polymerase results in the leading and lagging strands being synthesized differently
If the following nucleotide sequence, CTC/TGT/AAG/ACC/TTT experienced a mutation resulting in the deletion of the second cytosine in the first DNA triplet so the sequence is now CT_/TGT/AAG/ACC/TTT, what would be the amino acid sequence created from this mutated DNA strand? Table of mRNA codons UUA, UUG = leucine AGG, AGA = arginine %3D CAU, CAC = histidine GUU, GÜC, GUA = valine GAA. GAG=glutamic acid GCU, GUA, GUG = alanine GAU, GAC = asparagine GGU, GGC, GGA = glycine UCA, UCU =serine CGU, CGC, CGA = arginine
PolyADP-ribose polymerase (PARP) plays a keyrole in the repair of DNA single-strand breaks. In the pres-ence of the PARP inhibitor olaparib, single-strand breaksaccumulate. When a replication fork encounters a sin-gle-strand break, it converts it to a double-strand break,which in normal cells is then repaired by homologousrecombination. In cells defective for homologous recom-bination, however, inhibition of PARP triggers cell death.Patients who have only one functional copy of theBrca1 gene, which is required for homologous recombina-tion, are at much higher risk for cancer of the breast andovary. Cancers that arise in these tissues in these patientscan be treated successfully with olaparib. Explain how it isthat treatment with olaparib kills the cancer cells in thesepatients, but does not harm their normal cells.
5'-GCGGTACGTTACGGCTTTACTGACCTGCAGGC-3' A. Convert this to a double strand DNA molecule by writing the complementary sequence. Be sure to correctly label the ends of the double stranded molecule B. Pick one of the two strands and write the sequence of an RNA molecule that could be transcribed from it. Again, you must correctly label the ends of the molecule.
, describe the normal role of the component, and choose from the selection the most direct effect of the mutation and explain WHY. Choose from the 4 following effects: Initiation of DNA synthesis okazaki fragment synthesis Leading strand elongation lagging-strand completion --> Extracts from a strain of bacteria lacking the 5’ to 3’ exonuclease activity of DNA polymerase
Explain whether mismatch repair reduce the replication error if it is repaired without regard for which strand served as template.
A mutant DNA strand was transcribed then translated to proteins. a. What is the protein product of the mutant DNA strand? The sequence of the mutant strand is shown below: 5'-TGCCATAACTGTTCGTACTGGCAAATTGCC-3' 3'-ACGGTATTGACAAGCATGACCGTTTAACGG-5' b. The mutation altered the sequence of the wild type template DNA such that a degenerate codon for a basic amino acid in the wild type was converted to a non-degenerate codon resulting in the sequence for the mutant strand shown. What was the original amino acid? c. Compare the charges and pl of the mutant peptide and the normal (wild- type) peptide at physiological pH?
The mismatch DNA repair mechanism is based on the fact that: O a. O b. O C. O d. The parental DNA strand is recognized because it is structurally distorted. The parental DNA strand is methylated while daughter strand is not. The daughter DNA strand is recognized because it is structurally distorted. The daughter DNA strand is methylated while parental strand is not.
Translesion synthesis (TLS) polymerase zeta (ζ) is capable of accurately reading through 6,4-photoproducts (cytotoxic damage). If this protein is non-functional: a different TLS polymerase will accurately read through the DNA lesion. a different TLS polymerase will inaccurately read through the DNA lesion resulting in increased mutational frequency. the replicative polymerase will inaccurately read through the DNA damage. DNA polymerase alpha (α) will be recruited to synthesize a primer across the DNA damage. the DNA lesion cannot be bypassed and will result in double stranded DNA breaks.

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. It is thought that the signal for eukaryotic mismatch repair, for iden- tifying the strand to be repaired, could be nicks in the DNA to be repaired. If so, would you expect the nicked strand or the intact strand to be the strand to be repaired? Briefly explain your answer.