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2.3 DNA Damage & Repair β Test 1
Q1. A silent mutation:β Changes one DNA base without changing the amino acid sequence
Q2. Which enzyme repairs cyclobutane pyrimidine dimers directly?β DNA photolyase
Q3. Which is a DAMAGE-TOLERANCE (bypass) system rather than true repair?β SOS (translesion synthesis)
Q4. Xeroderma pigmentosum results from a defect in, and is associated with, which repair pathway?β Nucleotide excision repair
Q5. A frameshift mutation occurs when:β One or two (non-multiple-of-three) bases are inserted or deleted
Q6. A permanent, heritable alteration in DNA is called:β A mutation
Q7. Peroxides and metal ions (FeΒ²βΊ, CuΒ²βΊ) damage DNA mainly by:β Inducing single-strand breaks via oxidative attack on the backbone
Q8. UV-induced mutations are primarily due to:β Formation of thymine (pyrimidine) dimers
Q9. A point mutation changing codon UAC to UAU is a:β Silent mutation
Q10. Which repair mode tolerates damaged bases and continues DNA synthesis past them?β SOS (translesion) repair
Q11. A mutation is most likely to alter a protein's 3-D conformation if it:β Places proline in the middle of an Ξ±-helix
Q12. An E. coli strain lacking DNA polymerase I would be deficient in DNA:β Repair (and primer removal)
Q13. Base excision repair (BER) in human cells is mediated mainly by which DNA polymerase?β Pol Ξ²
Q14. Order of events during nucleotide excision repair (NER) in E. coli:β UvrAB, UvrC, DNA pol I, DNA ligase
Q15. During mismatch repair in E. coli, the correct series of events is:β MutS recognises the mismatch; MutH nicks at the unmethylated (new-strand) GATC; exonuclease/helicase remove the segment; Pol III resynthesizes; ligase seals
Q16. Error in nucleotide excision repair is a known cause of:β Xeroderma pigmentosum
Q17. How does the E. coli mismatch repair system identify the newly synthesized strand?β Old (parental) strand is methylated at GATC while the new strand is transiently unmethylated
Q18. In the case of a thymine dimer, what type of ring compound forms?β Cyclobutane
2.3 DNA Damage & Repair β Test 2
Q19. The mismatch repair system distinguishes parental from new strand because:β Adenine in the parental strand is methylated at GATC (hemimethylation)
Q20. Identify the mismatched repair pair:β UvrA β mismatch repair
Q21. If an enzyme produces, on average, one single-strand break per DNA molecule, the percentage of molecules left UNBROKEN (Poisson) is about:β 37%
Q22. If nucleotide A is replaced by G, the mutation is a:β Transition
Q23. In E. coli mismatch repair, the strand to be corrected is recognised by the presence of a nearby:β Hemimethylated GATC sequence
Q24. In Meselson-Stahl, after growth in ΒΉβ΅N then one generation in ΒΉβ΄N, the DNA is:β 50% ΒΉβ΅N / 50% ΒΉβ΄N hybrid (all intermediate density)
Q25. In Meselson-Stahl, after many generations in ΒΉβ΅N then TWO divisions in ΒΉβ΄N, what fraction has one light + one heavy strand?β 50%
Q26. Methylation of DNA (CpG, in promoters) generally results in:β Inactivation (silencing) of genes
Q27. Mutation in which protein abolishes recognition of mismatched base pairs in E. coli?β MutS
Q28. The E. coli repair system in which dual incisions remove a 12β13 base oligonucleotide is:β Nucleotide excision repair
Q29. People with Cockayne syndrome have a defective:β Transcription-coupled (NER) repair
Q30. Hydrogen-peroxide / peroxide-mediated DNA damage is detected by the presence of:β Single-strand breaks AND oxidized bases (oxidative damage)
Q31. Poly(ADP-ribose) polymerase (PARP) is needed for the repair of:β Single-stranded DNA breaks
Q32. Which mutagen predominantly causes frameshift mutations?β Acridine orange
Q33. The SOS response involves:β LexA cleavage (de-repression) leading to induction of repair genes
Q34. Statement (S): Missense mutations in p53 are common in cancers. Reason (R): loss of heterozygosity at p53 often promotes cancer. Choose:β S correct, R correct but not the explanation
Q35. Which property of telomerase DIFFERS from a typical DNA polymerase?β It carries its own internal RNA template (rather than using the DNA being copied)
Q36. The 'UvrABC' system repairs:β Bulky lesions/crosslinks and pyrimidine dimers (NER)
2.3 DNA Damage & Repair β Test 3
Q37. 5-Bromouracil causes mutations because it:β Replaces an A-T pair with G-C by tautomerizing and pairing with guanine
Q38. The function of UvrC in NER is to:β Catalyse incision(s) flanking the lesion
Q39. The mismatch repair system recognises the strand to repair via:β The hemimethylated GATC sequence nearby
Q40. Loss of an alkylated base by breakage of the bond between the purine and deoxyribose is termed:β Depurination
Q41. The UvrAB complex in E. coli excision repair recognises:β Pyrimidine dimers and other bulky lesions
Q42. Thymine dimers are formed through:β UV radiation
Q43. Types of DNA damage repairable by the E. coli DIRECT repair system include:β Alkylated bases (e.g. O6-methylguanine) and pyrimidine dimers
Q44. What role does p53 play in the DNA-damage response?β Acts as a transcription factor activating cell-cycle arrest, repair or apoptosis genes
Q45. Treating a cell with hydrogen peroxide causes which DNA damage?β Both single- and double-strand breaks (oxidative)
Q46. Which is a DNA crosslinking agent?β Psoralen
Q47. Which enzyme methylates hemimethylated DNA (maintenance methylation) in eukaryotes?β DNMT1
Q48. Which mutagen adds an alkyl group to guanine, causing direct mispairing with thymine?β EMS (ethyl methane sulfonate)
Q49. Which class of chemical mutagens is incorporated into DNA by the polymerase during replication?β Base analogues
Q50. Which statement about the SOS repair system is WRONG?β RecA permanently represses lexA
Q51. Which mutagen most likely causes a single amino-acid change (point/missense)?β Ethyl methane sulfonate (EMS)
Q52. Which enzyme carries out de novo methylation of DNA in mammals?β DNMT3a
Q53. Which one is NOT a DNA-depurinating agent?β Ethyl ethane sulphonate
Q54. Which is NOT involved in SOS repair?β UmuB
2.3 DNA Damage & Repair β Test 4
Q55. Which sequence of events correctly describes excision repair?β Recognition, nicking, excision, replacement, sealing
Q56. Which statement about base cross-linking is FALSE?β Cross-linked bases are always on opposing strands
Q57. Which transcription/repair factor functions in nucleotide excision repair in humans?β TFIIH
Q58. Xeroderma pigmentosum in humans is associated with a mutation affecting:β Nucleotide excision repair
Q59. You grow bacteria in ΒΉβ΅N then shift to ΒΉβ΄N for one generation; CsCl shows a single hybrid band between heavy and light. This indicates replication is:β Semi-conservative
Q60. One strand of dsDNA is mutated so all cytosines become uracils. After one round of replication of that strand, the Tm of the resulting duplex will:β Be lower
Q61. Which enzyme is responsible for maintenance methylation of hemimethylated DNA in eukaryotic cells?β DNMT1
Q62. X-rays induce mutagenic changes mainly by:β Chromosomal breakage (strand breaks)
Q63. The Kornberg enzyme (first DNA polymerase isolated) is:β DNA polymerase I
Q64. The Klenow fragment, generated by subtilisin treatment of Pol I, represents the:β C-terminal part of Pol I
Q65. Which DNA polymerase is used during base excision repair in human cells?β Pol Ξ²
Q66. Which has self-repairing mechanisms?β Only DNA
Q67. A mutation found ONLY in organisms with polycistronic mRNA is the:β Polar mutation
Q68. Which pathology can result from mutations affecting split-gene (splice-site) processing?β Ξ²-thalassaemia / cystic fibrosis (splice defects)
Q69. Genomic DNA from a normal person and a cancer patient was bisulfite-treated and PCR'd with promoter-specific primers. The assay studies:β DNA methylation status
Q70. Fidelity of base selection improved ~100-fold by editing; which enzyme/activity tolerates damage instead, lowering fidelity?β TLS (translesion) DNA polymerase
2.3 DNA Damage & Repair β Test 5
Q71. An inhibitor of FLAP endonuclease (FEN1) in NHEJ would most affect:β Gap/flap trimming during end processing
Q72. In sickle-cell detection, an allele-specific mutant probe hybridises stably to:β The homozygous mutant (Ξ²S/Ξ²S) gene
Q73. Rho, Tau and NusA are involved in:β Transcription
Q74. With increasing DNA damage/concentration, ATM kinase activity:β Increases, triggering cell-cycle checkpoints and repair
Q75. The arrangement (sequence/structure) of nucleotides in DNA was historically determined by:β X-ray crystallography/diffraction
Q76. During electrophoresis, the force moving DNA toward the anode is proportional to the number of:β Phosphate groups
Q77. The enzymes that use ATP hydrolysis to move along and melt double-stranded DNA are:β DNA helicase
Q78. The hydrophobic nature of a protein-nucleic acid interaction can be confirmed if the complex dissociates with:β Organic solvent
Q79. The number of subunits (polypeptide chains) in E. coli DNA polymerase I is:β 1
Q80. The 'refractory period' (delay before re-initiation) of E. coli replication is caused by:β A hemimethylated origin sequestered by SeqA
Q81. Which transcription factor with helicase activity participates in nucleotide excision repair?β TFIIH
Q82. The most correct general repair sequence for excision pathways is:β Recognition β incision β excision β resynthesis β ligation
Q83. A 'transition' mutation is defined as:β Purineβpurine or pyrimidineβpyrimidine substitution
Q84. O6-methylguanine, a mutagenic lesion, is repaired directly by:β O6-methylguanine-DNA methyltransferase (alkyltransferase)
Q85. Mismatch repair, if defective in humans, predisposes to:β Hereditary non-polyposis colorectal cancer (Lynch syndrome)
Q86. Direct reversal repair differs from excision repair because it:β Restores the original base/structure without removing nucleotides