Topoisomerases – Which statement about E. coli DNA gyrase is accurate?

Introduction:
DNA gyrase is a type II topoisomerase unique to bacteria that introduces negative supercoils into DNA, which is crucial for replication, transcription, and chromosome compaction. This question examines core functional and pharmacological properties of gyrase.

Given Data / Assumptions:

• Gyrase modulates DNA supercoiling state.
• Bacterial topoisomerases are targets of antibiotics (e.g., quinolones, fluoroquinolones).
• DNA transactions throughout the chromosome require supercoil management.

Concept / Approach:
Gyrase introduces negative supercoils and removes positive supercoils ahead of replication forks and transcription complexes. Fluoroquinolone antibiotics (e.g., ciprofloxacin) inhibit gyrase by stabilizing DNA–enzyme cleavage complexes, blocking religation and leading to lethal double-strand breaks. Gyrase is required globally, not just at oriC, and it is not a helicase (which unwinds duplex DNA by strand separation).

Step-by-Step Solution:

Verification / Alternative check:
Genetic and biochemical assays demonstrate accumulation of positive supercoils and growth arrest upon gyrase inhibition; quinolone resistance mutations map to gyrA/gyrB genes, confirming drug target identity.

Why Other Options Are Wrong:

• Adds positive supercoils: opposite of normal gyrase role.
• Only at oriC: gyrase acts genome-wide.
• Same as helicase: different enzymes; helicase separates strands, gyrase alters topology.
• Exclusively in transcription: it functions in multiple DNA processes.

Common Pitfalls:
Conflating supercoiling management (topoisomerases) with strand unwinding (helicases) or assuming gyrase is restricted to initiation sites.

Final Answer:
It can be inhibited by specific antibiotics (e.g., quinolones).