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3.2 Transposition Mechanisms & Control â Test 1
Q1. Bacteriophage Mu is notable because it:â Uses transposition as its mechanism of replication and integration
Q2. Phage Mu replicates its genome during the lytic cycle mainly by:â Replicative transposition
Q3. The Tn3 element controls its own transposition frequency through:â Resolvase (TnpR) acting as a repressor of the transposase gene
Q4. Tn10 down-regulates its own transposition using:â Antisense RNA (RNA-OUT pairing with RNA-IN) that blocks transposase translation
Q5. Tn10 transposition is also influenced by Dam methylation, which:â Couples transposition to passage of the replication fork (hemimethylated state activates it)
Q6. Multicopy inhibition of Tn10 means that:â Increasing element copy number decreases transposition per element (via antisense RNA)
Q7. In Mu transposition, the transposase is encoded by gene:â MuA
Q8. The accessory protein MuB functions to:â Deliver/capture target DNA and stimulate strand transfer (ATP-dependent)
Q9. 'Transposition immunity' (target immunity) ensures that:â A transposon avoids inserting into a DNA molecule that already contains a copy
Q10. Replicative transposition (e.g. Tn3, Mu) proceeds through a key intermediate called the:â Cointegrate
Q11. DDE transposases (like MuA) are named for:â A catalytic triad of two aspartates and a glutamate that coordinates Mg²âº
Q12. Cut-and-paste transposases create a hairpin or double-strand break by:â Cleaving both strands at the transposon ends to excise the element
Q13. After cut-and-paste excision of Tn10, the donor site is:â Left with a double-strand break that the host must repair
Q14. The heat-shock response in E. coli that can influence stress-related gene expression uses the regulator:â ϳ² (ÏH, RpoH) sigma factor
Q15. Why is tight regulation of transposition advantageous for the host-element relationship?â Excessive transposition would damage the host genome, harming both host and element survival
Q16. Strand transfer in transposition refers to:â Joining of the transposon 3'-OH ends to the target DNA
Q17. Phage Mu integrates into the host genome at:â Essentially random target sites (hence its mutagenic nature)
Q18. A key difference between replicative and conservative transposition is that replicative transposition:â Increases element copy number (one copy stays, one is made at the target)
Q19. Antisense RNA control of Tn10 (RNA-OUT) works by:â Base-pairing with the transposase mRNA to occlude its ribosome-binding site
Q20. In the Tn3 family, the control logic is best described as:â tnpA + tnpR, where TnpR represses transposase and resolves cointegrates