Molecular Biology of the Cell: DNA Replication and Repair

These flashcards review key concepts from the DNA replication and repair lecture, covering the roles and mechanisms of critical enzymes, types of DNA damage, and repair processes.

What are the capabilities and limitations of DNA polymerase?

DNA polymerase can add nucleotides based on complementary base pairing and creates phosphodiester bonds, but it cannot initiate DNA synthesis.

What is the concept of replication origin?

Replication origin is the specific location where DNA replication begins, differing between prokaryotes (one origin) and eukaryotes (multiple origins).

Why is DNA polymerase not able to unwind the DNA helix?

DNA polymerase cannot unwind the helix, necessitating additional proteins such as helicase and topoisomerase at the replication fork.

What is semi-conservative replication?

Semi-conservative replication is a process where each new double helix is made of one parent strand and one newly synthesized strand.

What role does telomerase play in DNA replication?

Telomerase extends the 3' ends of chromosomes in continuously dividing cells to prevent loss of DNA during replication.

Describe the mechanism of proofreading by DNA polymerase.

Proofreading is done by DNA polymerase's 3'-5' nuclease activity, allowing it to remove incorrectly paired nucleotides.

What is the difference between base excision repair and mismatch repair?

Base excision repair removes and replaces damaged bases, while mismatch repair corrects mispaired bases during DNA synthesis.

What types of DNA damage can result in mutations if not repaired?

Base substitutions and frameshift mutations can arise from improper or unrepaired DNA damage.

Explain the processes of non-homologous end joining and homologous recombination.

Non-homologous end joining is error-prone and can lead to nucleotide loss, while homologous recombination is error-free and uses a sister chromatid for accurate repair.

What is the significance of BRCA1 and BRCA2 mutations in cancer risk?

Mutations in BRCA1 and BRCA2 increase the lifetime risk of breast and ovarian cancer due to impaired DNA repair mechanisms.