During replication, helicase unwinding increases positive supercoiling ahead of the fork. Which protein primarily causes this overwinding, and which enzyme removes it to allow fork progression?

Introduction / Context:
DNA replication imposes topological stress. As helicase opens the duplex, positive supercoils accumulate ahead of the fork, potentially stalling progression. Topoisomerases resolve this stress. This question asks you to pair the cause of overwinding with the enzyme that relieves it.

Given Data / Assumptions:

• DnaB is the primary replicative helicase in many bacteria.
• Positive supercoils arise ahead of the fork during unwinding.
• DNA gyrase is a type II topoisomerase that can introduce negative supercoils and remove positive supercoils.

Concept / Approach:
Helicase action is the proximate cause of overwinding (rotational constraint ahead of the fork). Gyrase transiently breaks both strands, passes another segment through, and reseals, thereby relaxing positive supercoils and enabling fork movement.

Step-by-Step Solution:

Verification / Alternative check:
Inhibition of gyrase (e.g., by quinolones) causes replication fork arrest due to unresolved supercoils, confirming its role.

Why Other Options Are Wrong:

• DnaB, DNA polymerase: polymerase does not resolve supercoils.
• DnaA, DNA gyrase: DnaA initiates origin melting; it is not the main cause of ongoing overwinding at the fork.
• SSB, DnaA: SSB stabilizes single strands; neither resolves supercoils.
• Primase, DNA ligase: primer synthesis and nick sealing do not manage topology.

Common Pitfalls:
Confusing initiation (DnaA) with elongation dynamics; assuming ligase or polymerase relieve torsional strain—this is topoisomerase work.

Final Answer:
DnaB (helicase), DNA gyrase (topoisomerase II)