# Molecular Biology Basics > Molecular biology basics for FMGE Biochemistry: DNA structure, replication, repair syndromes, transcription blockers, genetic code and mutations in notes. - Canonical URL: https://prepelephant.com/topics/fmge/biochemistry/molecular-basics-fmge - Exam / course: FMGE · Subject: Biochemistry - Publisher: PrepElephant (https://prepelephant.com) — Prepared and reviewed by the PrepElephant Academic Review Team - First published: 2026-10-02 - Last updated: 2026-10-02 - How to cite: "Molecular Biology Basics", PrepElephant, https://prepelephant.com/topics/fmge/biochemistry/molecular-basics-fmge ## Direct answer DNA stores information in base pairs held between two antiparallel strands — adenine with thymine through two hydrogen bonds, guanine with cytosine through three — arranged in a double helix 2 nm wide with 10 base pairs and a 3.4 nm rise per turn. Replication is semi-conservative, demonstrated by Meselson and Stahl's heavy-nitrogen experiment, continuous on the leading strand and discontinuous on the lagging strand as Okazaki fragments sealed by DNA ligase, with polymerases proofreading in the 3' to 5' direction. Transcription by RNA polymerase II builds messenger RNA from the template strand, and translation reads the triplet code — 64 codons, degenerate and non-overlapping, AUG as start and UAA, UAG and UGA as stops — on ribosomes. ## What you must remember - Chargaff's rule: within any species A equals T and G equals C; A-plus-T-rich regions denature first. - DNA polymerase III is the workhorse replicase of prokaryotes with 3' to 5' proofreading exonuclease activity; eukaryotic telomerase, a reverse transcriptase carrying its own RNA template, restores chromosome ends in germ cells and most cancers. - Drug probes examiners recycle: rifampicin inhibits the β subunit of bacterial RNA polymerase (the basis of anti-tubercular therapy), α-amanitin from Amanita phalloides inhibits eukaryotic RNA polymerase II, and actinomycin D intercalates into DNA to block transcription. - Repair syndromes: xeroderma pigmentosum — nucleotide excision repair of ultraviolet pyrimidine dimers; Lynch syndrome — mismatch repair; BRCA1 and 2 — homologous recombination of double-strand breaks; ataxia-telangiectasia — ATM signalling of double-strand breaks. - Mutation vocabulary with named examples: silent; missense (HbS, glutamate to valine); nonsense or premature stop (some β0 thalassaemias); frameshift (a cystic fibrosis example is not ΔF508, which deletes three bases in frame — a classic trap); splice-site variants. - The nucleosome wraps about 200 base pairs around a histone octamer of two each of H2A, H2B, H3 and H4, with H1 sealing the linker DNA; acetylation of histone tails opens chromatin for transcription. - Codon anchors: AUG starts every reading frame coding methionine, UGG is tryptophan, and degeneracy concentrates at the third, wobble position — the molecular basis for silent polymorphisms. ## From gene to gel: the sickle mutation walked through Take the β-globin gene and change one letter — the codon GAG becomes GTG, an A-to-T transversion. Transcription copies the change faithfully, translation reads GUG as valine, and the sixth position of the β chain, which should carry a negatively charged glutamate, now carries a hydrophobic valine. That single charge change is visible on a gel: at alkaline pH on cellulose acetate, haemoglobin moves toward the anode at a speed set by its net charge, and HbS, having lost one negative charge, migrates more slowly than HbA — the principle behind sickle screening, with high-performance liquid chromatography and solubility tests now doing the quantitation. The pathogenicity is structural: the surface valine fits a hydrophobic pocket formed on a partner haemoglobin by its Phe85 and Leu88 when deoxygenated, so the molecules stack into fibres that deform the erythrocyte. Every level of the central dogma sits inside this one mutation, which is why it anchors half the molecular biology the exam asks. ## Where students slip Rifampicin and α-amanitin are swapped — one blocks the bacterial enzyme, the other the human RNA polymerase II; tie rifampicin to tuberculosis and amanitin to the death-cap mushroom. Second, the ΔF508 cystic fibrosis deletion is called a frameshift; deleting exactly three bases keeps the reading frame, making it an in-frame deletion. Third, semi-conservative is defined loosely; it means each daughter double helix retains one intact parental strand, which is precisely what the Meselson–Stahl density gradient showed. Fourth, the leading strand needs one primer while the lagging strand needs one per Okazaki fragment, so ligase works only on the lagging strand. Fifth, the wobble hypothesis explains why codon third-position changes are often silent — a point that converts several "which mutation is silent" stems from guesswork to logic. Finally, cytosine deamination creates uracil, which is why DNA uses thymine as a checkpoint against mutation. ## Frequently asked questions ### Which experiment established semi-conservative replication? Meselson and Stahl grew Escherichia coli in heavy nitrogen-15, shifted it to nitrogen-14, and showed daughter DNA of intermediate density — one old strand, one new. ### Which antibiotic inhibits bacterial RNA polymerase, and how is that exploited? Rifampicin, by binding the β subunit; selective bacterial toxicity underlies its use against tuberculosis and leprosy. ### Which repair defect underlies xeroderma pigmentosum? Failure of nucleotide excision repair to remove ultraviolet-induced pyrimidine dimers, producing freckling, photosensitivity and early skin cancers. ### What are the three stop codons? UAA, UAG and UGA — none codes for an amino acid, and release factors terminate the chain. ### What mutation type is sickle-cell haemoglobin? A missense transversion (GAG to GTG) replacing glutamate with valine at β6, detectable as slower anodal migration on electrophoresis. ### How many base pairs occupy one turn of the B-DNA helix? Ten, spanning 3.4 nm of rise, in a helix 2 nm in diameter — the three numbers every viva asks.