Podcast
Questions and Answers
What is the immediate consequence when a DNA replication fork encounters a lesion in the DNA template, and it bypasses it?
What is the immediate consequence when a DNA replication fork encounters a lesion in the DNA template, and it bypasses it?
Which of the following describes a scenario where a lesion in the template strand does not necessarily stall the replication fork?
Which of the following describes a scenario where a lesion in the template strand does not necessarily stall the replication fork?
What is the most frequent immediate outcome when the replisome encounters a lesion in the DNA template before repair?
What is the most frequent immediate outcome when the replisome encounters a lesion in the DNA template before repair?
What directly leads to the collapse of the replication fork, creating a double strand break?
What directly leads to the collapse of the replication fork, creating a double strand break?
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How does translesion synthesis (TLS) differ from normal DNA replication?
How does translesion synthesis (TLS) differ from normal DNA replication?
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What is the significance of an O-meG base in the template strand for DNA replication?
What is the significance of an O-meG base in the template strand for DNA replication?
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Which process is required to restore an undamaged replication fork following a double-strand break resulting from a stalled replication fork?
Which process is required to restore an undamaged replication fork following a double-strand break resulting from a stalled replication fork?
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Why is damage to DNA considered to be highly deleterious?
Why is damage to DNA considered to be highly deleterious?
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What is the immediate consequence of a DNA lesion that blocks the replication machinery but allows it to resume further downstream?
What is the immediate consequence of a DNA lesion that blocks the replication machinery but allows it to resume further downstream?
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Why is a lesion in the lagging strand more easily bypassed by the replication machinery?
Why is a lesion in the lagging strand more easily bypassed by the replication machinery?
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What is the initial step in the recombinational repair of a double-strand break (DSB)?
What is the initial step in the recombinational repair of a double-strand break (DSB)?
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What is the role of the homologous DNA molecule in double-strand break (DSB) repair?
What is the role of the homologous DNA molecule in double-strand break (DSB) repair?
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What is the key characteristic of the strand invasion process during homologous recombination?
What is the key characteristic of the strand invasion process during homologous recombination?
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What is the significance of using the 3' ends for single strand invasion?
What is the significance of using the 3' ends for single strand invasion?
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What is a 'D-loop' in the context of recombinational DNA repair?
What is a 'D-loop' in the context of recombinational DNA repair?
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What is the main difference between how DNA polymerase works in synthesis dependent strand annealing (SDSA), and general replication?
What is the main difference between how DNA polymerase works in synthesis dependent strand annealing (SDSA), and general replication?
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In synthesis-dependent strand annealing (SDSA), what happens to the lengthened invading strands after extension by the DNA polymerase?
In synthesis-dependent strand annealing (SDSA), what happens to the lengthened invading strands after extension by the DNA polymerase?
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Which of the following enzymes is NOT directly involved in the early stages of recombinational DNA repair of a double strand break?
Which of the following enzymes is NOT directly involved in the early stages of recombinational DNA repair of a double strand break?
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Study Notes
DNA Damage and Replication
- DNA damage is common and harmful. Consequences appear during replication.
- Replication can continue over a lesion (translesion synthesis, TLS). Specialized polymerases aid TLS.
- Normally, only specialized polymerases perform TLS. Regular polymerases might replicate some lesions without significant distortion.
- A lesion can also stop replication, requiring repair before continuing or restart replication further downstream.
- Replication can halt if a repair process is happening when a lesion is encountered. This can lead to a replication fork collapse and double-strand breaks.
- Recombinational DNA repair restores the replication fork structure and allows replication to restart.
- Most lesions cause the replication fork to stall. Replication ceases until repaired.
- The replication machinery may bypass the lesion and resume downstream of the lesion.
- This bypass plus restart phenomenon is frequent when the lesion is in the lagging strand.
Double-Strand Breaks (DSBs)
- DSBs occur due to oxidative DNA damage, oxygen-rich environments, or ionizing radiation.
- DSBs are destructive and usually lethal if not repaired.
- DSBs can arise from a broken template strand encountered by a replication fork during repair.
- Recombination repairs DSBs. Repair requires a homologous, undamaged DNA molecule.
- The repair DNA guides restoration of information lost at the break.
- Repair initiation involves three enzymatic reactions:
- Processing broken ends to create single-stranded extensions (overhangs)
- Strand invasion of the homologous chromosome.
- Replicative extension of the invading strand.
Recombinational DNA Repair Process
- Enzymes process broken DNA ends into 3' single-stranded extensions (overhangs).
- Recombinase enzymes facilitate strand invasion of the homologous chromosome.
- The invading strands are extended by DNA polymerases.
- Several pathways resolve the "double crossover" intermediate, one of which is synthesis-dependent strand annealing (SDSA).
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Description
Explore the critical concepts surrounding DNA damage and its impact on replication. This quiz covers the mechanisms like translesion synthesis and the role of specialized polymerases in managing lesions. Understand the implications of replication fork stalling and the processes involved in DNA repair.