Bio111 Exam 2- Module 14- TAMU- Fletcher

🧬 MOLECULAR GENETICS – STUDY NOTES


Part 1: Key Experiments and Discoveries

🧪 Griffith (1928) – Transformation

  • Studied Streptococcus pneumoniae in mice.

  • Found that harmless (R) bacteria could be transformed into deadly (S) bacteria when mixed with heat-killed S strain.

  • Concluded: a ā€œtransforming principleā€ (later found to be DNA) transferred genetic information.

🧬 Avery, MacLeod, & McCarty (1944)

  • Repeated Griffith’s work in vitro (in test tubes).

  • Treated samples with enzymes that destroyed proteins, RNA, or DNA.

  • Only when DNA was destroyed did transformation not occur.

  • Conclusion: DNA is the genetic material.

☢ Hershey & Chase (1952)

  • Used bacteriophages (viruses that infect bacteria).

  • Labeled DNA with radioactive phosphorus (³²P) and protein with radioactive sulfur (³⁵S).

  • Only ³²P (DNA) entered bacteria.

  • Proved: DNA, not protein, carries genetic info.

🧮 Chargaff (1950)

  • Analyzed DNA composition across species.

  • Found that A = T and G = C (base pairing rule).

  • Known as Chargaff’s Rule.

šŸ’Ž Wilkins & Franklin (1952)

  • Used X-ray crystallography to photograph DNA.

  • Franklin’s photo showed an X-shaped pattern, indicating a double helix structure.

🧩 Watson & Crick (1953)

  • Built the first 3D model of DNA.

  • Combined Chargaff’s rules and Franklin’s X-ray data.

  • Determined the double helix structure: sugar-phosphate backbone on the outside, base pairs inside (A-T, G-C).


Part 2: DNA Structure & Organization

Structure of Double-Stranded DNA

  • Components: Sugar (deoxyribose), phosphate group, nitrogenous base (A, T, G, C).

  • Arrangement: Two antiparallel strands forming a double helix.

  • Base pairing: A–T (2 hydrogen bonds), G–C (3 hydrogen bonds).

  • Importance: Enables accurate replication and information storage.

Nucleotide Percentages

  • A = T, G = C, and A + T + G + C = 100%.
    Example: If A = 30%, then T = 30%, G = 20%, C = 20%.

DNA Packaging

  • Histones: Positively charged proteins that DNA wraps around.

  • Nucleosomes: ā€œBeads on a stringā€ (DNA + histone).

  • Chromatin: DNA-protein complex that folds into higher-order structures to fit in the nucleus.

  • Importance: Compacts DNA and regulates gene expression.

Euchromatin vs. Heterochromatin

  • Euchromatin: Loosely packed, active genes, seen during interphase.

  • Heterochromatin: Densely packed, inactive genes, often near centromeres/telomeres.

  • Dynamic — can switch forms to control gene activity.


Part 3: DNA Replication

Main Enzymes & Their Roles

Enzyme

Function

Helicase

Unzips DNA strands by breaking hydrogen bonds.

Single-Strand Binding Proteins (SSBPs)

Hold strands apart (ā€œdoorstopsā€).

Topoisomerase

Relieves tension and prevents supercoiling ahead of replication fork.

Primase

Adds short RNA primers for DNA polymerase to start synthesis.

DNA Polymerase

Adds complementary bases, proofreads, works 5’ → 3’.

DNA Ligase

ā€œSealsā€ gaps between Okazaki fragments on lagging strand.

Leading vs. Lagging Strand

  • Leading strand: Synthesized continuously (5’ → 3’).

  • Lagging strand: Synthesized discontinuously in short Okazaki fragments due to opposite direction (3’ → 5’).

  • DNA polymerase can only add nucleotides to the 3’ end.

End Replication Problem

  • Eukaryotic chromosomes are linear, and lagging strand synthesis leaves a small gap at the 3’ end.

  • Telomeres: Repetitive, noncoding DNA sequences at chromosome ends that protect genes.

  • Telomerase: Enzyme that extends telomeres, active in stem cells and cancer cells.


Part 4: Mutation Prevention & DNA Repair

Mutation Prevention

  1. Proofreading (DNA Polymerase):

    • During replication, fixes mismatched bases instantly.

  2. Nucleotide Excision Repair (NER):

    • After replication, removes and replaces damaged DNA sections (e.g., from UV light).

Telomeres & Telomerase

  • Telomeres: Repetitive DNA protecting chromosome ends.

  • Telomerase: Enzyme that adds telomere repeats.

  • Active in germ cells, stem cells, and cancer cells, allowing continuous division.

  • Most somatic cells have inactive telomerase → aging and cell death.

Consequences of Unfixed Errors

  • Mutations: permanent DNA sequence changes.

  • Can be beneficial, neutral, or harmful.

  • Some cause diseases or cancer.

Types of Mutations

Type

Description

Example/Effect

Point Mutation

One base change

Substitution → silent, missense, or nonsense

Frameshift Mutation

Insertion or deletion shifts reading frame

Alters entire protein sequence

Chromosomal Mutation

Large-scale changes (duplication, deletion, inversion, translocation)

Affects many genes