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4.3 DNA Repair, Suppression & Mutation Equilibrium β Test 1
Q1. When adenine spontaneously converts to hypoxanthine, creating a mismatch, the base-excision-repair enzymes that correct it are:β Glycosylase/AP-nuclease, DNA polymerase and DNA ligase
Q2. The original source of new alleles of genes in a population is:β Mutation
Q3. The mutation theory of evolution was proposed by:β Hugo de Vries
Q4. A second mutation within the same gene that restores the wild-type phenotype is called:β Intragenic suppression
Q5. A tRNA-gene mutation in the anticodon that allows it to read a nonsense (stop) codon and complete translation is a:β Nonsense suppressor
Q6. A nonsense mutation's effect can be cancelled by either true reversion or a suppressor. These two kinds of revertants are distinguished by:β Recombination (genetic crossing)
Q7. Xeroderma pigmentosum is caused by a genetic defect in:β Nucleotide-excision repair
Q8. XP patients cannot repair UV-induced thymine dimers, most directly because of a defective:β Excision endonuclease (NER)
Q9. In E. coli mismatch repair, the parental (template) strand is distinguished from the new strand by:β Methylation of adenine in GATC sequences
Q10. A premature-ageing syndrome linked to defects in genome-maintenance/structural genes is:β HutchinsonβGilford progeria
Q11. UV-induced pyrimidine dimers can be directly reversed (without excision) by the enzyme:β DNA photolyase (photoreactivation)
Q12. The base-excision-repair enzyme that removes uracil arising from cytosine deamination is:β Uracil-DNA glycosylase
Q13. The SOS repair system in E. coli is best described as:β An error-prone, damage-inducible response
Q14. Mismatch repair in E. coli is initiated by the protein that recognises the mismatched base pair, namely:β MutS
Q15. At an autosomal locus, A1 mutates to A2 at ΞΌ = 1Γ10β»β΅ and A2 mutates to A1 at Ξ½ = 2Γ10β»β΅. The equilibrium frequency of A1 is:β 0.67
Q16. Defective human mismatch-repair genes (e.g. MSH2, MLH1) are most associated with:β Hereditary non-polyposis colorectal cancer (Lynch syndrome)
Q17. Alkylation damage such as O6-methylguanine is directly reversed by:β O6-methylguanine-DNA methyltransferase (a 'suicide' enzyme)
Q18. An intergenic suppressor differs from a true revertant in that the suppressor:β Lies in a different gene and can be separated by recombination
Q19. Translesion synthesis (TLS) polymerases allow replication past DNA lesions but are:β Low-fidelity and potentially mutagenic
Q20. Match each repair pathway with its target/feature and select the correct option.β A-iii, B-i, C-ii, D-iv