1. Which of the following is a DNA repair mechanism that corrects mismatches during DNA replication?
a) Base Excision Repair (BER)
b) Nucleotide Excision Repair (NER)
c) Mismatch Repair (MMR)
d) Homologous Recombination (HR)
Answer: c) Mismatch Repair (MMR)
Explanation: Mismatch Repair (MMR) corrects mismatches that occur during DNA replication by identifying and repairing incorrect base pairings.
2. Which type of DNA repair is responsible for fixing small base lesions, such as those caused by oxidative damage?
a) Base Excision Repair (BER)
b) Nucleotide Excision Repair (NER)
c) Mismatch Repair (MMR)
d) Homologous Recombination (HR)
Answer: a) Base Excision Repair (BER)
Explanation: Base Excision Repair (BER) removes and replaces small, damaged bases caused by oxidation, alkylation, or deamination.
3. Which of the following DNA repair mechanisms is involved in the repair of bulky lesions, such as those caused by UV radiation?
a) Base Excision Repair (BER)
b) Nucleotide Excision Repair (NER)
c) Mismatch Repair (MMR)
d) Homologous Recombination (HR)
Answer: b) Nucleotide Excision Repair (NER)
Explanation: Nucleotide Excision Repair (NER) removes bulky lesions like thymine dimers caused by UV radiation.
4. What type of DNA damage is repaired by Homologous Recombination (HR)?
a) Single-strand breaks
b) Double-strand breaks
c) Base pair mismatches
d) Bulky adducts
Answer: b) Double-strand breaks
Explanation: Homologous Recombination (HR) repairs double-strand breaks in DNA by using a homologous template to restore the sequence.
5. Which gene mutation is associated with a higher risk of developing certain cancers due to impaired DNA repair?
a) TP53
b) BRCA1/BRCA2
c) MYC
d) Ras
Answer: b) BRCA1/BRCA2
Explanation: Mutations in BRCA1 and BRCA2 impair the homologous recombination repair pathway, significantly increasing the risk of breast and ovarian cancers.
6. The gene TP53, often mutated in cancers, encodes a protein that:
a) Promotes DNA repair
b) Stimulates apoptosis in response to DNA damage
c) Acts as a transcription factor for DNA repair genes
d) All of the above
Answer: d) All of the above
Explanation: TP53 is a tumor suppressor gene that promotes DNA repair, triggers apoptosis when damage is irreparable, and activates genes involved in DNA repair processes.
7. Which of the following is a key component of the Mismatch Repair (MMR) pathway?
a) p53
b) BRCA1
c) MLH1
d) RAD51
Answer: c) MLH1
Explanation: MLH1 is a critical component of the Mismatch Repair (MMR) pathway, where it forms complexes to correct mismatched DNA base pairs.
8. What is the primary function of the DNA repair mechanism called ‘Nucleotide Excision Repair’ (NER)?
a) Repairing oxidative DNA damage
b) Correcting base pair mismatches
c) Removing bulky DNA lesions
d) Repairing single-strand breaks
Answer: c) Removing bulky DNA lesions
Explanation: Nucleotide Excision Repair (NER) removes bulky DNA lesions such as thymine dimers or other distortions caused by environmental factors like UV radiation.
9. A defect in the DNA repair process of non-homologous end joining (NHEJ) is primarily associated with:
a) Increased UV sensitivity
b) Predisposition to leukemia and lymphoma
c) Reduced risk of colon cancer
d) Increased likelihood of BRCA mutations
Answer: b) Predisposition to leukemia and lymphoma
Explanation: Defects in NHEJ, which repairs double-strand breaks, are linked to increased susceptibility to cancers, particularly blood cancers like leukemia and lymphoma.
10. Which DNA repair pathway is typically used to repair double-strand breaks during the cell cycle’s S and G2 phases?
a) Non-homologous end joining (NHEJ)
b) Homologous recombination (HR)
c) Base excision repair (BER)
d) Nucleotide excision repair (NER)
Answer: b) Homologous recombination (HR)
Explanation: Homologous recombination (HR) is the preferred repair mechanism for double-strand breaks during the S and G2 phases of the cell cycle, where a homologous template is available.
11. The DNA damage response (DDR) pathway helps prevent cancer by:
a) Promoting cell cycle progression
b) Inducing DNA repair mechanisms or apoptosis
c) Activating tumor growth genes
d) Inhibiting transcription factors
Answer: b) Inducing DNA repair mechanisms or apoptosis
Explanation: The DNA damage response (DDR) pathway activates repair mechanisms or initiates apoptosis in response to DNA damage to prevent mutations and cancer.
12. A key function of the ATM protein in DNA repair is:
a) Activating the p53 tumor suppressor gene
b) Initiating the repair of double-strand breaks
c) Stimulating the synthesis of cyclins
d) Facilitating base excision repair
Answer: b) Initiating the repair of double-strand breaks
Explanation: The ATM (ataxia-telangiectasia mutated) protein detects double-strand breaks and activates pathways involved in their repair, including homologous recombination.
13. What is the result of a defect in the gene that encodes the protein BRCA1?
a) Reduced ability to repair single-strand breaks
b) Increased risk of developing cancer due to defective DNA repair
c) Increased production of antioxidants
d) Enhanced tumor suppressor activity
Answer: b) Increased risk of developing cancer due to defective DNA repair
Explanation: BRCA1 is involved in repairing double-strand breaks via homologous recombination. A defect in BRCA1 leads to increased genomic instability and a higher risk of breast and ovarian cancers.
14. Which of the following is NOT a common result of defective DNA repair mechanisms in human cells?
a) Increased mutation rates
b) Genomic instability
c) Improved DNA replication accuracy
d) Cancer development
Answer: c) Improved DNA replication accuracy
Explanation: Defective DNA repair mechanisms increase mutation rates, cause genomic instability, and contribute to cancer development. They do not improve replication accuracy.
15. Which of the following best describes the role of p53 in DNA repair?
a) Activates repair enzymes directly
b) Initiates the repair of damaged DNA
c) Induces cell cycle arrest or apoptosis in response to DNA damage
d) Promotes the replication of damaged DNA
Answer: c) Induces cell cycle arrest or apoptosis in response to DNA damage
Explanation: p53 acts as a tumor suppressor by halting the cell cycle or initiating apoptosis in response to DNA damage, preventing the propagation of damaged cells.
16. Which DNA repair mechanism is associated with the correction of deaminated cytosine to uracil?
a) Mismatch repair (MMR)
b) Base excision repair (BER)
c) Nucleotide excision repair (NER)
d) Homologous recombination (HR)
Answer: b) Base excision repair (BER)
Explanation: Base excision repair (BER) fixes small lesions like deamination of cytosine, which results in the incorporation of uracil in place of cytosine.
17. The presence of which of the following proteins in the repair of DNA damage often determines whether the cell undergoes repair or apoptosis?
a) Caspase
b) p53
c) BRCA1
d) RAD51
Answer: b) p53
Explanation: p53 is a critical protein that decides whether the cell will attempt to repair DNA damage or undergo apoptosis if the damage is irreparable.
18. Which condition is associated with defects in the nucleotide excision repair (NER) pathway?
a) Xeroderma pigmentosum
b) Ataxia-telangiectasia
c) Fanconi anemia
d) Bloom syndrome
Answer: a) Xeroderma pigmentosum
Explanation: Xeroderma pigmentosum is caused by mutations in the NER pathway, leading to an inability to repair UV-induced DNA damage, resulting in skin cancers.
19. How do DNA repair mechanisms prevent cancer?
a) By eliminating mutated cells
b) By reducing the mutation rate and maintaining genome stability
c) By stimulating the expression of oncogenes
d) By activating apoptosis of healthy cells
Answer: b) By reducing the mutation rate and maintaining genome stability
Explanation: DNA repair mechanisms reduce mutation rates and maintain genome integrity, preventing the accumulation of mutations that could lead to cancer.
20. In the process of nucleotide excision repair (NER), what happens to the damaged segment of DNA?
a) It is methylated
b) It is excised and replaced with the correct sequence
c) It is phosphorylated
d) It is transcribed
Answer: b) It is excised and replaced with the correct sequence
Explanation: In NER, the damaged DNA segment is excised, and the gap is filled by DNA polymerase, using the undamaged strand as a template.
21. What role do DNA ligases play in DNA repair?
a) They act as sensors for DNA damage
b) They remove damaged bases
c) They rejoin broken DNA strands after repair
d) They initiate the repair process
Answer: c) They rejoin broken DNA strands after repair
Explanation: DNA ligases seal the nicks in the DNA backbone after repair, ensuring that the strands are rejoined.
22. Which of the following statements about non-homologous end joining (NHEJ) is true?
a) It repairs single-strand breaks
b) It is the primary repair mechanism for double-strand breaks in the G1 phase
c) It requires a homologous template for repair
d) It functions only in the S phase
Answer: b) It is the primary repair mechanism for double-strand breaks in the G1 phase
Explanation: Non-homologous end joining (NHEJ) is the main repair mechanism for double-strand breaks in the G1 phase when homologous recombination is unavailable.
23. How does BRCA2 contribute to DNA repair?
a) By promoting base excision repair
b) By facilitating homologous recombination repair of double-strand breaks
c) By triggering apoptosis
d) By synthesizing new DNA strands
Answer: b) By facilitating homologous recombination repair of double-strand breaks
Explanation: BRCA2 facilitates homologous recombination by helping to load RAD51 onto single-stranded DNA at sites of double-strand breaks.
24. Which type of DNA repair mechanism is activated by the detection of oxidative DNA damage?
a) Mismatch repair (MMR)
b) Base excision repair (BER)
c) Homologous recombination (HR)
d) Nucleotide excision repair (NER)
Answer: b) Base excision repair (BER)
Explanation: Base excision repair (BER) is activated by oxidative DNA damage, where damaged bases such as oxidized guanine are removed and replaced.
25. What effect does ionizing radiation have on DNA that requires repair?
a) Induces single-strand breaks only
b) Causes double-strand breaks and complex lesions
c) Causes mutations in base pairs
d) Alters chromatin structure
Answer: b) Causes double-strand breaks and complex lesions
Explanation: Ionizing radiation can cause double-strand breaks and complex lesions, which are repaired by pathways like homologous recombination and non-homologous end joining.
26. The Fanconi anemia pathway is most important for repairing which type of DNA damage?
a) Double-strand breaks
b) UV-induced thymine dimers
c) Interstrand crosslinks
d) Single-strand breaks
Answer: c) Interstrand crosslinks
Explanation: The Fanconi anemia pathway is crucial for repairing interstrand crosslinks that can interfere with DNA replication.
27. Which DNA repair pathway is most often associated with repair during the G1 phase of the cell cycle?
a) Homologous recombination (HR)
b) Base excision repair (BER)
c) Non-homologous end joining (NHEJ)
d) Nucleotide excision repair (NER)
Answer: c) Non-homologous end joining (NHEJ)
Explanation: Non-homologous end joining (NHEJ) is the primary mechanism for repairing double-strand breaks in the G1 phase of the cell cycle.
28. In response to DNA damage, p53 acts to:
a) Repair the DNA directly
b) Induce cell cycle arrest or apoptosis
c) Synthesize repair enzymes
d) Stimulate the production of free radicals
Answer: b) Induce cell cycle arrest or apoptosis
Explanation: p53 activates cell cycle checkpoints or induces apoptosis in response to DNA damage, preventing the replication of damaged DNA.
29. A mutation in the DNA repair gene MLH1 is associated with which cancer syndrome?
a) Lynch syndrome
b) Li-Fraumeni syndrome
c) Fanconi anemia
d) Retinoblastoma
Answer: a) Lynch syndrome
Explanation: Mutations in the MLH1 gene are associated with Lynch syndrome, which increases the risk of colon cancer due to defective mismatch repair.
30. Which of the following is a consequence of DNA damage accumulating in a cell without repair?
a) Enhanced DNA replication accuracy
b) Increased genomic instability and cancer risk
c) Improved cellular function
d) Faster cell division
Answer: b) Increased genomic instability and cancer risk
Explanation: Accumulated DNA damage leads to genomic instability, which increases the risk of mutations and cancer development.
