Eukaryotic linear chromosomes face the end-replication problem. Which mechanism primarily resolves this limitation at chromosome ends?

Introduction / Context:
Lagging-strand synthesis near chromosome termini cannot fully replicate the 3' ends after primer removal. This is known as the end-replication problem.

Given Data / Assumptions:

• Linear eukaryotic chromosomes have telomeres composed of short repeats.
• Conventional DNA polymerases need a primer and cannot extend 3' ends without it.

Concept / Approach:
Telomerase, a ribonucleoprotein reverse transcriptase, uses its internal RNA as template to extend the 3' overhang, allowing completion of complementary strand synthesis and maintenance of telomere length.

Step-by-Step Solution:
1) Telomerase binds the 3' end and aligns its RNA template with telomeric DNA.2) It adds repeat units to the 3' end via reverse transcription.3) DNA polymerase then fills the complementary strand using a primer synthesized by primase.

Verification / Alternative check:
Cells lacking telomerase show progressive telomere shortening and replicative senescence; telomerase reactivation stabilizes telomeres.

Why Other Options Are Wrong:
Deliberate shortening does not solve the problem; the entire chromosome is not copied from RNA template; “none” is incorrect since telomerase is the established mechanism.

Common Pitfalls:
Confusing telomerase RNA as a general genome template rather than a short repeat template at ends.

Final Answer:
Using the enzyme telomerase