AHL: DNA replication extensions
IB Biology HLΒ· D1.1 DNA replication AHL extensionsΒ· 20 min read
1. Multiple Replication Originsβ β ββββ± 5 min
Replication Origin
A specific DNA sequence where helicase first binds to unwind the double helix and initiate DNA replication.
Example:
Prokaryotes have one circular chromosome and a single replication origin.
Prokaryotes have small, circular genomes, so one replication origin is sufficient to complete replication in a reasonable time. Eukaryotes have much larger linear genomes: a single human chromosome is hundreds of millions of base pairs long, so replication from a single origin would take weeks, which is impractical.
Eukaryotes solve this by having thousands of replication origins across all their chromosomes, allowing replication to proceed simultaneously from many points, completing the entire genome in hours.
Compare the number of replication origins in E. coli (prokaryote) and human (eukaryote) cells, and explain why this difference exists.
- 1
E. coli has a single 4.6 million base pair circular chromosome, so it only needs one replication origin. Bidirectional replication from this origin completes the whole genome in ~40 minutes.
- 2
Human cells have 46 linear chromosomes with a total of ~6 billion base pairs. Replication from one origin per chromosome would take ~30 days per chromosome.
- 3
Humans have ~100,000 replication origins across all chromosomes, enabling simultaneous replication that completes the entire genome in ~8 hours.
2. Telomeres and Telomeraseβ β β βββ± 6 min
Telomere
Repetitive non-coding DNA sequences at the ends of linear eukaryotic chromosomes that protect coding DNA from being lost during replication.
The end replication problem arises because when the final RNA primer on the lagging strand is removed, there is no 3' hydroxyl end to add DNA nucleotides to fill the gap. This means a short segment of DNA is lost from the chromosome end every replication cycle.
Telomerase extends the 3' end of telomeres by adding new repetitive sequences, compensating for this loss. Telomerase is active in germ cells, stem cells, and most cancer cells, but inactive in most somatic cells, leading to gradual telomere shortening over divisions.
Explain why prokaryotes do not need telomeres.
- 1
Prokaryotic chromosomes are circular, so they have no free ends.
- 2
The end replication problem only occurs at the free ends of linear chromosomes, where the final RNA primer cannot be replaced.
- 3
No free end means no unreplaced gap, no DNA is lost, so telomeres are unnecessary.
Exam tip:
IB exams frequently ask to link telomerase activity to cancer: active telomerase lets cancer cells divide indefinitely.
3. DNA Proofreadingβ β ββββ± 4 min
Proofreading
A 3'β5' exonuclease activity of DNA polymerase that checks each new nucleotide against the template and removes mismatched bases before continuing replication.
Even with complementary base pairing, DNA polymerase makes a mistake roughly once every 100,000 nucleotides. Proofreading reduces this error rate to ~1 per 10 million nucleotides, drastically increasing replication fidelity.
Predict the effect on mutation rate if DNA polymerase loses its proofreading activity.
- 1
Proofreading is the primary mechanism that removes mismatched nucleotides during replication.
- 2
Without proofreading, the frequency of mismatched bases would increase ~100-fold compared to normal replication.
- 3
This results in a much higher mutation rate, increasing the risk of deleterious mutations that disrupt protein function.
4. Post-Replication Mismatch Repairβ β β β ββ± 5 min
Proofreading does not catch all replication errors. Mismatch repair is a post-replication mechanism that corrects remaining mismatches, insertions, and deletions. This reduces the final error rate to ~1 per 1 billion nucleotides.
Mismatch Repair
A post-replication repair pathway that corrects errors missed by proofreading, maintaining genome stability.
How does E. coli distinguish the new incorrect strand from the original template strand during mismatch repair?
- 1
In E. coli, the original template strand is methylated at adenine residues in GATC sequences.
- 2
Immediately after replication, the new strand is not yet methylated, so mismatch repair enzymes can identify which strand contains the error.
- 3
The segment of new strand with the mismatch is removed and resynthesized using the template, after which the new strand is methylated.
5. Common Pitfalls
Wrong move:
Claiming DNA is lost from both chromosome ends every replication cycle
Why:
Only the 5' end of the lagging strand has an unreplaced gap after primer removal. The 3' end extends fully to the chromosome end.
Correct move:
Explain that the end replication problem causes gradual telomere shortening because the final lagging strand primer cannot be replaced with DNA.
Wrong move:
Stating that all human cells have active telomerase
Why:
Most somatic human cells turn off telomerase activity after differentiation.
Correct move:
Telomerase is only active in germ cells, stem cells, and most cancer cells.
Wrong move:
Claiming prokaryotes do not have proofreading or DNA repair
Why:
Prokaryotes also experience replication errors and require mechanisms to maintain genome fidelity.
Correct move:
Both prokaryotes and eukaryotes use proofreading and mismatch repair to reduce replication error rates.
Wrong move:
Attributing multiple replication origins only to slower eukaryotic replication speed
Why:
The primary driver is the much larger size of eukaryotic genomes compared to prokaryotes.
Correct move:
Multiple replication origins enable simultaneous replication of large eukaryotic genomes, reducing total replication time.
6. Quick Reference Cheatsheet
Feature | Prokaryotes | Eukaryotes |
|---|---|---|
Replication origins | 1 per chromosome | 100s-1000s per chromosome |
Chromosome shape | Circular | Linear |
End replication problem | None | Occurs |
Telomeres present | No | Yes |
Telomerase active | No | Only in germ/stem/cancer cells |
Proofreading activity | Yes | Yes |
Mismatch repair | Yes | Yes |
7. Frequently Asked
Do I need to memorize detailed molecular steps of DNA repair?
No. IB Biology HL only requires you to outline the purpose of proofreading and mismatch repair, and explain why they are necessary, not full molecular details.
When this came up on past exams
AI-estimated based on syllabus patterns β cross-check with official past papers for accuracy. Use only as revision-focus signals.
- 2025 Β· 1
Telomere function multiple choice
- 2023 Β· 2
Telomerase and cancer extended response
- 2021 Β· 1
DNA repair explanation question
Going deeper
What's Next
Understanding DNA replication extensions is foundational for studying mutations, cancer, and genetic variation, all core topics in IB Biology HL. Telomere shortening and telomerase activity are regularly linked to aging and cancer development, while mutations in DNA repair genes are strongly associated with genetic disorders and elevated cancer risk. Replication fidelity and mutation rate also underpin evolutionary biology, as new mutations are the source of genetic variation that natural selection acts on. Build on these concepts by exploring transcription, mutation, and cancer biology next.