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Unit 5 • DNA & Expression

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Directionality: always annotate strands 5'→3'; lagging strand issues drive telomerase story.
Mutation consequences: nonsense vs missense vs frameshift; relate to cancer genes (p53, Rb).
Chromatin states: euchromatin (loose, active) vs heterochromatin (tight, silent).
Virus life cycles: lytic vs lysogenic; retroviral reverse transcriptase error-prone → rapid evolution.

DNA vs RNA

Sugar

DNA: deoxyribose (no 2' OH) → stable; RNA: ribose (2' OH) → reactive.

Bases

DNA: A, T, C, G; RNA: A, U, C, G.

Strands

DNA: double helix, antiparallel; RNA: mostly single-stranded, can fold into hairpins.

Role

DNA stores; RNA acts (mRNA, tRNA, rRNA, snRNA, miRNA) + catalysis (ribozyme).

RNA Roles & Transcription/Translation

mRNA

Carries genetic message; codons specify amino acids; template for translation.

tRNA

Brings specific amino acid; anticodon pairs with mRNA codon.

rRNA

Ribosome catalyst; forms peptide bond; structural scaffold with proteins.

Prok vs Euk

  • • Transcription in nucleus, translation in cytoplasm; linear chromosomes; mRNA processed (cap, tail, splicing); introns removed.
  • • Both in cytoplasm; circular DNA; no introns; transcription/translation coupled.

DNA Replication

1

Helicase unwinds; topoisomerase relieves supercoils ahead of fork.

2

Single-strand binding proteins stabilize unwound strands.

3

Primase lays RNA primers.

4

DNA polymerase III extends 5'→3' from primers (leading continuous; lagging Okazaki).

5

DNA polymerase I replaces RNA primers with DNA; ligase seals sugar-phosphate backbone.

6

Proofreading + mismatch repair correct errors; ligase finishes nicks.

Telomerase extends lagging strand ends (germline, stem cells, cancer). DNA pol reads 3'→5', builds 5'→3'.

Replication Enzymes (order)

1

Helicase: unwinds double helix.

2

SSB proteins: keep strands apart.

3

Primase: lays RNA primers.

4

DNA pol III: extends leading + lagging strands.

5

DNA pol I: replaces RNA primers with DNA.

6

Ligase: seals sugar-phosphate backbone.

Leading: one primer. Lagging: many primers → Okazaki fragments.

DNA pol vs RNA pol

Direction built

Both synthesize 5'→3' and move along template 3'→5'.

Primer

DNA pol needs primer; RNA pol does not.

Proofreading

DNA pol proofreads; RNA pol lacks strong proofreading → more errors tolerated.

Helicase

DNA pol needs helicase; RNA pol can unwind small regions itself.

RNA pol errors tolerated; DNA pol proofreads to protect genomes.

Mutations & Stops

Missense

Point mutation → new amino acid; impact depends on chemistry/position.

Nonsense

Point mutation → stop codon; truncates protein.

Silent

Point mutation → same amino acid; can still affect splicing/translation speed rarely.

Frameshift

Indel not multiple of 3 shifts reading frame → early stop, altered amino acids.

Release factor (protein) ends translation at stop codon; genetic code is degenerate.

Central Dogma & Expression

Transcription (nucleus): RNA polymerase binds promoter (with transcription factors) → mRNA.
RNA processing (euk): 5' cap, poly-A tail, splicing out introns.
Translation (cytosol/RER): ribosome reads mRNA; tRNAs bring amino acids; peptide bonds via peptidyl transferase.
Protein targeting: signal peptides send proteins to ER, mitochondria, or remain cytosolic.

Chromatin: euchromatin = active; heterochromatin = silent. Histone acetylation generally activates; DNA methylation often silences.

Gene Expression Control

DNA level

Methylation condenses/silences; histone acetylation opens chromatin → transcription.

Transcription factors

General (TATA-binding protein) vs specific (enhancer-binding activators/repressors).

Post-transcription

5' cap + poly-A tail for protection/export/ribosome binding; alternative splicing for isoforms.

Post-translation

Cleavage, phosphorylation, glycosylation, ubiquitin to change activity, location, stability.

ncRNA

miRNA/siRNA can degrade mRNA or block ribosome binding; lncRNA can alter chromatin.

Genetic code is degenerate; release factor (not tRNA) stops translation at stop codon.

Cell Cycle & Cancer

G1: growth; G1/S checkpoint evaluates size, nutrients, DNA integrity.
S: DNA replication.
G2: prep for mitosis; G2/M checkpoint checks replication completion + DNA damage.
M: mitosis + cytokinesis; spindle checkpoint ensures proper kinetochore attachment.

Cancer genes

  • • Proto-oncogenes (e.g., Ras, Myc): gain-of-function mutations → uncontrolled growth signaling.
  • • Tumor suppressors (e.g., p53, Rb, BRCA): loss-of-function disables checkpoints/repair.
  • • Mutagens/carcinogens: radiation, chemicals, viruses increase mutation rate; telomerase reactivation supports immortality.

Cancer logic

  • • Growth-promoting; gain-of-function (dominant) mutations → stuck ON (e.g., Ras).
  • • Brake proteins; loss-of-function (recessive) mutations disable checkpoints (p53, Rb, BRCA).
  • • Normal cells stop with crowding or no attachment; cancer often ignores both.

Extras

  • • G1 size/nutrients/DNA damage; G2 replication complete; M spindle attachment.
  • • Programmed cell death if damage persists; cancer often evades.
  • • From centrosomes; attach kinetochores, align in metaphase, shorten in anaphase.
  • • Cohesin holds sisters; separase cleaves at anaphase; actin ring pinches in cytokinesis.
  • • Density-dependent inhibition; anchorage dependence.

G1

Checks size, nutrients, DNA damage; p53 can halt for repair or trigger apoptosis.

G2

Ensures DNA replication completed, damage repaired before mitosis.

M (spindle)

Verifies kinetochores attached to spindle before separating chromatids.

Viruses & Prions

Core virus facts

  • • Obligate intracellular; capsid ± envelope.
  • • Lytic: rapid replication → host lysis.
  • • Lysogenic: genome integrates (prophage/provirus); can later enter lytic.
  • • RNA viruses often use RNA-dependent RNA polymerase; retroviruses use reverse transcriptase → DNA → integration.
  • • Vaccines prime adaptive immunity; antivirals target entry, replication, assembly, or release.

Host range

Viral surface proteins must match specific host cell receptors; defines species + tissue tropism.

Genome types

DNA or RNA, single- or double-stranded. RNA genomes rely on RNA polymerases (no host proofreading) → higher mutation.

Virus-first

Self-assembled before cells; independent origin.

Reductionist

Cells downsized under pressure; stripped genomes/proteins.

Escape

Escaped genes/cassettes acquired capsids and became parasites.

Viral polymerases

  • • RNA-dependent RNA polymerase copies RNA genome using RNA template; not encoded by host.
  • • Makes DNA from viral RNA, inserts into host genome; error-prone.

Prions

  • • Protein-only; no nucleic acid.
  • • Misfolded β-sheet-rich proteins induce misfolding of normal proteins → aggregates.
  • • Aggregates kill neurons; resistant to heat/acid—no easy deactivation.