Replication Mechanics Under Stress
This experimental result disproved both conservative and dispersive replication models after one generation in ¹⁴N medium.
A single DNA band of intermediate density in the Meselson–Stahl experiment
This protein recognizes ATP‑bound initiator complexes to begin replication at oriC.
DnaA
This methylation enzyme modifies adenine within GATC sequences to regulate replication timing.
Dam methyltransferase
UV light most commonly produces this type of covalent DNA lesion.
Thymine dimers
This repair process directly reverses damage without removing nucleotides from the DNA backbone.
Direct repair
DNA polymerase III synthesizes DNA rapidly but cannot initiate synthesis because it lacks this molecular requirement.
A free 3′‑OH provided by an RNA primer
The helicase loader is released after this replication step is successfully completed.
DnaB loading onto single‑stranded DNA
Immediately after replication, oriC exists in this methylation state.
Hemimethylation
This spontaneous reaction converts cytosine into uracil, increasing transition mutations.
Deamination
Removal of a damaged base followed by incision at an AP site defines this repair pathway.
Base excision repair
If helicase activity were inhibited while primase remained functional, this immediate consequence would occur at the replication fork.
Failure to generate single‑stranded DNA templates
oriC is A‑T rich because this physical property lowers the energetic cost of initiation.
Fewer hydrogen bonds between base pairs
This protein prevents premature re‑initiation by binding hemimethylated oriC.
SeqA
This oxidative lesion frequently mispairs with adenine during replication.
8‑oxoguanine
This repair system removes bulky UV‑induced lesions by excising ~24–32 nucleotides.
Nucleotide excision repair
The antiparallel structure of DNA directly explains the necessity of this replication feature on one strand.
Okazaki fragments
Replication forks stop only when approaching ter sites from one direction due to this protein’s polarity.
Tus
Conversion of DnaA‑ATP to this inactive form helps ensure replication occurs only once per cell cycle.
DnaA‑ADP
Intercalating agents primarily cause this mutation type by distorting DNA spacing.
Frameshift mutations
This damage‑tolerance process allows replication past lesions but increases mutation risk.
Translesion synthesis
Explain why lagging‑strand synthesis is discontinuous even though DNA synthesis always proceeds 5′→3′.
Strand antiparallel orientation relative to replication fork movement
After replication completion, this enzyme is required to resolve interlinked daughter chromosomes.
Topoisomerase IV
Compare bacterial initiation control to eukaryotic replication licensing in terms of origin usage.
Single regulated origin per chromosome versus multiple licensed origins that fire once per cycle?
Ionizing radiation is particularly lethal because it generates this difficult‑to‑repair lesion.
Double‑strand breaks
This bacterial emergency response promotes survival by inducing low‑fidelity polymerases through LexA cleavage.
The SOS response