Replication is semiconservative (Meselson-Stahl) and bidirectional; polymerases synthesize only 5′→3′ from a free 3'-OH, so primase must lay RNA primers.
Enzyme order: helicase unwinds, topoisomerase (gyrase) relieves supercoils ahead, SSB proteins hold strands apart, DNA Pol III extends, DNA Pol I replaces primers, ligase seals nicks.
The leading strand runs continuously toward the fork; the lagging strand builds Okazaki fragments away from it, each with its own primer.
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Linear chromosomes shorten each division (end replication problem); telomerase, a reverse transcriptase with an internal RNA template, extends TTAGGG repeats in stem, germ, and cancer cells.
Accuracy improves stepwise: Pol III alone∼10−5→proofreading∼10−7→mismatch repair∼10−9
Repair Pathways
Mismatch repair fixes post-replication errors (defect: Lynch syndrome). Base excision repair handles deaminated or oxidized bases. Nucleotide excision repair removes bulky lesions like UV thymine dimers (defect: xeroderma pigmentosum). Double-strand breaks use accurate homologous recombination (BRCA1/2, needs a sister chromatid) or error-prone NHEJ.
Key Takeaways
Memorize the enzyme sequence at the fork and why the lagging strand is discontinuous.
Telomerase activity separates immortal cells from aging somatic cells.
Match each repair pathway to its lesion and its disease.
HR is template-guided and faithful; NHEJ just glues ends.