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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
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The DNA Replication Fork01:02

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An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
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The basic reaction of homologous recombination (HR) involves two chromatids that contain DNA sequences sharing a significant stretch of identity. One of these sequences uses a strand from another as a template to synthesize DNA in an enzyme-catalyzed reaction. The final product is a novel amalgamation of the two substrates. To ensure an accurate recombination of sequences, HR is restricted to the S and G2 phases of the cell cycle. At these stages, the DNA has been replicated already and the...
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In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
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Making Choices: DNA Replication Fork Recovery Mechanisms.

Christine M Kondratick1, M Todd Washington1,2, Maria Spies1,2

  • 1Department of Biochemistry, Carver College of Medicine, University of Iowa, Iowa City, Iowa 52242.

Seminars in Cell & Developmental Biology
|May 10, 2021
PubMed
Summary

DNA replication forks face obstacles, triggering repair or bypass mechanisms. This review explores key proteins and processes involved in DNA damage response, highlighting risks to genome integrity.

Keywords:
BRCA2DNA replicationHLTFPCNARAD51RAD52RPASHPRHSMARCAL1ZRANB3genome stabilityreplication fork protectionreplication fork reversaltemplate switchingtranslesion synthesistranslesion synthesis DNA polymerases

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA replication forks encounter numerous obstacles that can stall, collapse, or break them.
  • Cells employ complex mechanisms to bypass, repair, or restart damaged replication forks.
  • Understanding these mechanisms is crucial for comprehending genome stability and disease development.

Purpose of the Study:

  • To review the molecular mechanisms of DNA damage bypass and replication fork protection and repair.
  • To highlight key protein players that dictate the cellular response to replication stress.
  • To discuss the inherent risks to genome integrity associated with these DNA repair pathways.

Main Methods:

  • Literature review focusing on molecular mechanisms of DNA replication and repair.
  • Analysis of key proteins involved in replication fork dynamics and stress response.
  • Discussion of posttranslational modifications, DNA polymerases, and recombination machinery.

Main Results:

  • Identified key players including PCNA, translesion synthesis polymerases, fork reversal motors, and homologous recombination machinery.
  • Described how these proteins coordinate to protect and repair stalled replication forks.
  • Highlighted the potential for normal repair intermediates to trigger aberrant processes leading to genomic instability.

Conclusions:

  • Faithful genome duplication relies on intricate coordination of DNA damage response pathways.
  • Dysregulation of these pathways can lead to cancer, cell death, and therapeutic resistance.
  • Further research is needed to fully elucidate the selection and regulation of these critical DNA repair mechanisms.