GMT20240315-024414_Recording_1728x1118
Chapter 6: DNA Replication and Repair
6.1 Overview of Variations in DNA
Differences in DNA produce variations among individuals of the same species.
Over evolutionary time, genetic changes lead to species distinctions (e.g., different hair colors in a family).
Variations in traits are underpinned by underlying genetic differences.
6.2 DNA Replication
6.2.1 Base Pairing and Template Function
DNA acts as a template for its own replication.
Base pairs: A pairs with T, G pairs with C.
Each strand has a primary (S strand) and a complementary strand (S' strand).
DNA sequences read from 5' to 3' direction; complementary strands read in opposite 5' to 3' direction.
6.2.2 Semiconservative Replication
DNA replication is semiconservative: each daughter DNA has one old strand and one newly synthesized strand.
DNA synthesis begins at the origin of replication, where initiator proteins unwind the DNA double helix.
6.2.3 Models of DNA Replication
Semiconservative Model: Each new DNA molecule contains one old and one new strand.
Dispersive Model: DNA molecules contain segments of both old and new DNA.
Conservative Model: Original DNA strand remains intact while an entirely new strand is synthesized.
6.2.4 Experimental Evidence
Meselson and Stahl Experiments: Used cesium chloride gradient centrifugation to demonstrate semiconservative replication by showing intermediate density of the replicated molecules.
6.2.5 Replication Forks and Directionality
Two replication forks form at each origin and move in opposite directions.
Leading strand heads toward the replication fork while the lagging strand moves away, forming Okazaki fragments.
6.3 DNA Polymerase and Synthesis Direction
DNA polymerase synthesizes new strands in the 5' to 3' direction.
Incoming nucleoside triphosphates form base pairs with the template strands.
The replication fork is asymmetrical.
Lagging strand synthesized in short Okazaki fragments using a back stitching mechanism.
6.3.1 Proofreading by DNA Polymerase
DNA polymerase has proofreading ability, correcting errors by removing mispaired nucleotides as they are detected.
Different sites within the polymerase enzyme are dedicated to synthesis and proofreading functions.
6.3.2 Role of RNA Primase
RNA primers synthesized by RNA polymerase (primase) are necessary to start DNA replication.
Primase synthesizes RNA primers that are approximately 10 nucleotides long.
6.4 Enzymes and Proteins in DNA Replication
Essential enzymes include:
DNA Polymerases: Synthesize new strands and proofread.
RNA Primase (Primase): Synthesizes RNA primers.
DNA Ligase: Joins Okazaki fragments; functions like "glue".
Helicase: Unwinds the DNA double helix.
Topoisomerase: Relieves the torsional stress during unwinding.
Single-Strand Binding Proteins: Protect single-stranded DNA.
6.5 Telomerase and Chromosome Ends
Telomeres are GC-rich sequences at chromosome ends; telomerase extends these ends during DNA replication to prevent loss of sequences.
Critical for maintaining chromosome integrity during cell division.
6.6 DNA Repair Mechanisms
6.6.1 Types of DNA Damage
Depurination (loss of purine bases) and deamination (conversion of cytosine to uracil) lead to common DNA damages.
UV radiation can cause thymine dimers, linking adjacent thymine bases covalently.
6.6.2 DNA Repair Steps
Excision: Damaged nucleotides are removed by nucleases.
Resynthesis: DNA polymerase fills in the gaps using the complementary strand as a template.
Ligation: DNA ligase seals any remaining breaks in the DNA backbone.
6.7 Mismatch Repair System
A repair mechanism that targets replication errors missed by proofreading.
Corrects single nucleotide mismatches that may result in permanent mutations if not repaired.
6.8 Double-Strand Break Repair
Double-strand breaks are repaired via:
Non-Homologous End Joining: Quick repair but may cause deletions.
Homologous Recombination: Preferred method that does not result in loss of nucleotides.
6.9 Consequences of DNA Repair Failures
Failure to repair can lead to mutations, potential diseases (e.g., sickle cell anemia), or genomic instability.
Importance of fidelity in DNA replication and repair is evidenced by comparisons of DNA sequences among organisms.