COMPETITIVE EXAM MCQs SERIES of LIFE SCIENCES for UGC-CSIR NET/JRF, SLET, GATE, and other entrance tests: FUNDAMENTAL PROCESSES – DNA Replication and Repair.
Syllabus Outline
- Mechanisms of DNA replication.
- Enzymes involved in replication (e.g., DNA polymerases (I, II, III), helicases, primases, ligases, topoisomerases)
- Replication origin and replication fork (oriC in prokaryotes, eukaryotic multiple origins, replication bubble and fork dynamics)
- Fidelity of replication (Proofreading, mismatch repair, role of exonucleases).
- Extrachromosomal replicons (Plasmids, mitochondrial and chloroplast DNA, viral replicons).
- Types of DNA damage (e.g., UV, oxidative and chemical)
- DNA repair mechanisms (e.g., direct repair, base excision repair, nucleotide excision repair, mismatch repair)
This quiz contains concept-based, most frequently asked 25 MCQs of “FUNDAMENTAL PROCESSES – DNA Replication and Repair”. Each question has a single correct/most appropriate answer.
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1. The transition from the Pre-Replicative Complex to the Pre-Initiation Complex marks the onset of S-phase. Which complex represents the active eukaryotic replicative helicase?
A) The MCM2-7 double hexamer.
B) The ORC-Cdc6-Cdt1 complex.
C) The CMG complexes.
D) The PCNA-RFC complex.
2. Geminin is a critical regulator of genomic stability in metazoans. What is its primary molecular function?
A) It phosphorylates MCM proteins to activate them.
B) It prevents the recruitment of MCM helicases to origins.
C) It acts as a primase for the leading strand.
D) It degrades the ORC complex.
3. A researcher overexpresses non-degradable Cdc6 and Cdt1 in human cells during the G2 phase. What phenotype is most likely to be observed?
A) Premature entry into Mitosis.
B) Endoreduplication.
C) Inhibition of all DNA synthesis.
D) Activation of the Apoptosis pathway due to a lack of origins.
4. In the eukaryotic replication fork, “Polymerase Switching” refers to:
A) The transition from leading strand synthesis to lagging strand synthesis.
B) The replacement of Pol delta with Pol zeta during replication.
C) The switch from DNA polymerase to RNA polymerase during transcription.
D) The replacement of Pol alpha-primase with Pol delta or Pol epsilon.
5. A yeast strain with a mutation in the catalytic subunit of Pol II shows an increased mutation rate specifically on the leading strand. A similar mutation in Pol III causes mutations primarily on the lagging strand. This data supports which model?
A) Pol II and Pol III function redundantly on both strands.
B) Pol III is the leading strand replicase, and Pol II is the lagging strand replicase.
C) Pol III replicates the leading strand, and Pol II replicates the lagging strand.
D) Pol II is the leading strand replicase, and Pol III is the lagging strand replicase.
6. Which eukaryotic replication factor acts as the “Sliding Clamp,” topologically encircling DNA to tether polymerases?
A) Replication Factor C
B) Replication Protein A
C) Proliferating Cell Nuclear Antigen
D) Mini-Chromosome Maintenance complex
7. Replication Factor C is the eukaryotic “Clamp Loader.” Its function is dependent on:
A) ATP binding and hydrolysis.
B) GTP hydrolysis.
C) Phosphorylation by CDK.
D) The presence of RNA primers only.
8. Aphidicolin is a specific inhibitor of eukaryotic nuclear DNA replication. Which enzyme(s) does it primarily inhibit?
A) DNA Polymerases
B) DNA Primase
C) Mitochondrial Polymerase
D) Bacterial Polymerase III.
9. In eukaryotic Okazaki fragment maturation, what is the consequence of a defect in FEN1 activity?
A) Failure to synthesise the RNA primer.
B) Accumulation of DNA fragments with 5′ flaps.
C) Inability of Pol delta to displace the strand.
D) Immediate arrest of leading strand synthesis.
10. Which enzymatic activity is present in E. coli DNA Polymerase I but absent in eukaryotic Pol delta and Pol epsilon, necessitating the use of FEN1?
A) 5’→3′ Polymerase activity.
B) 3’→5′ Exonuclease activity.
C) 5’→3′ Exonuclease activity.
D) Helicase activity.
11. Why is Replication Protein A inhibitory to FEN1 activity on long flaps?
A) Replication Protein A induces a conformational change in the DNA that blocks the FEN1 active site.
B) Replication Protein A induce proteases to degrade FEN1 before it can act.
C) Replication Protein A recruits Ligase before FEN1 can act.
D) Replication Protein A makes the flap double-stranded DNA that prevent binding of FEN1
12. Which eukaryotic DNA ligase is primarily responsible for sealing Okazaki fragments during replication?
A) Ligase I
B) Ligase III
C) Ligase IV
D) Ligase V
13. Telomerase is best described as:
A) A DNA-dependent DNA polymerase.
B) An RNA-dependent DNA polymerase.
C) A DNA-dependent RNA polymerase.
D) An RNA-dependent RNA polymerase.
14. Dyskeratosis Congenita is a disease associated with bone marrow failure. Many cases are caused by mutations in the gene encoding dyskerin. What is the fundamental cellular defect?
A) Defective Nucleotide Excision Repair.
B) Inability to maintain telomere length.
C) Overactive Homologous Recombination.
D) Failure of the spindle checkpoint.
15. How does the human Mismatch Repair system distinguish the newly synthesised strand from the template strand?
A) By the absence of methylation on the new strand, while the template strand is methylated.
B) By the presence of RNA primers.
C) By the phosphorylation of Histone H2AX.
D) By the orientation of the Proliferating Cell Nuclear Antigen clamp on the new strand.
16. Hereditary Non-Polyposis Colorectal Cancer is primarily caused by germline mutations in which class of genes?
A) Nucleotide Excision Repair genes.
B) Mismatch Repair genes.
C) Double-Strand Break Repair genes.
D) Base Excision Repair genes.
17. Which enzyme activity distinguishes DNA Polymerase beta in the Base Excision Repair pathway?
A) 3’→5′ Exonuclease activity.
B) 5′ Deoxyribose Phosphate Lyase activity.
C) RNA Primase activity.
D) Helicase activity.
18. Xeroderma Pigmentosum Variant is caused by a defect in Pol. Why do these patients have a high incidence of skin cancer?
A) They cannot repair UV dimers.
B) Their cells undergo apoptosis too easily.
C) They have a defect in Telomerase.
D) They bypass UV dimers.
19. The “Klenow Fragment” of E. coli DNA Pol I lacks which activity?
A) 5’→3′ Polymerase.
B) 3’→5′ Exonuclease.
C) 5’→3′ Exonuclease.
D) DNA binding.
20. The high processivity of E. coli DNA Polymerase III is due to the beta sliding clamp. Which thermodynamic event drives loading of the beta clamp onto DNA?
A) Spontaneous association of beta monomers around DNA through hydrophobic interactions
B) ATP hydrolysis by the tau subunit to propel the clamp.
C) Binding of ATP to the gamma complex to open the beta clamp.
D) Phosphorylation of the beta clamp by primase.
21. A temperature-sensitive mutation occurs in the dnaC gene of E. coli. At the restrictive temperature, which step of DNA replication initiation is primarily blocked?
A) Melting of AT-rich repeats at the origin of replication
B) Synthesis of the RNA primer
C) Loading of the DnaB helicase onto single-stranded DNA
D) Binding of DnaA protein to origin recognition sequences
22. Why does coli DNA ligase use NAD+ as a cofactor, while bacteriophage T4 DNA ligase uses ATP?
A) Concentration of NAD+ is higher than ATP in bacteria, whereas viruses contain a higher concentration of ATP as compared to NAD+ due to the low maintenance required.
B) Bacterial ligases evolved a distinct adenylation mechanism using NAD+
C) NAD+ releases more energy than ATP
D) Viral ligases requires low-energy for functioning as compared to bacterial ligases.
23. Which DNA repair pathway predominates during the G1 phase of the cell cycle?
A) Homologous recombination
B) Non-homologous end joining
C) Break-induced replication
D) Single-strand annealing
24. Mono-ubiquitination of Proliferating Cell Nuclear Antigen primarily signals:
A) Translesion synthesis polymerase recruitment.
B) DNA damage checkpoint activation.
C) Template switching.
D) Replication origin firing.
25. Assertion (A): The gamma-complex of the Pol III holoenzyme is termed an AAA+ ATPase.
Reason (R): It utilises the energy of ATP hydrolysis to remodel the beta-clamp, opening the ring interface to allow DNA entry.
A) Both A and R are true, and R is the correct explanation of A.
B) Both A and R are true, but R is not the correct explanation of A.
C) A is true, but R is false.
D) A is false, but R is true.
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References
- Nelson, David L. & Cox, Michael M. (2021). Lehninger Principles of Biochemistry, W. H. Freeman, 8th Edition.
- Cooper, G. M. (2022). The Cell: A Molecular Approach, Sinauer Associates, 9th Edition
- Kumar, P., & Mina, U. (2025). Life Sciences: Fundamentals and Practice – Part I & II, Pathfinder Academy, 9th Edition
- Verma, P. S., & Agarwal, V. K. (2022). Cell Biology, Genetics, Molecular Biology, Evolution and Ecology, S. Chand Publishing, 1st Edition
- Alberts, B., Johnson, A., Lewis, J., Morgan, D., Raff, M., Roberts, K., & Walter, P. (2014). Molecular Biology of the Cell, Garland Science, 6th Edition.
- Gupta, P.K. (2022). Cell and Molecular Biology, Rastogi Publications, 5th Edition.
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