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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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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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Homologous Recombination02:31

Homologous Recombination

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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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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
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DNA Damage can Stall the Cell Cycle02:37

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In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
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Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
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Updated: Jun 23, 2025

Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence
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Quantifying Replication Stress in Ovarian Cancer Cells Using Single-Stranded DNA Immunofluorescence

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MRNIP limits ssDNA gaps during replication stress.

Laura G Bennett1, Ellen G Vernon1, Vithursha Thanendran1

  • 1North West Cancer Research Institute, North Wales Medical School, Bangor, Gwynedd, Wales LL57 2UW, UK.

Nucleic Acids Research
|June 25, 2024
PubMed
Summary
This summary is machine-generated.

The MRE11 regulator MRNIP prevents DNA gaps during replication stress, particularly when fork reversal is impaired. MRNIP deficiency increases sensitivity to PARP inhibitors and DNA damage.

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Detection of Post-Replicative Gaps Accumulation and Repair in Human Cells Using the DNA Fiber Assay
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Area of Science:

  • Molecular Biology
  • DNA Replication
  • DNA Repair

Background:

  • Replication stress can lead to DNA gaps, impacting genome stability.
  • PRIMPOL-dependent repriming creates single-stranded DNA (ssDNA) gaps, linked to mutagenesis and chemosensitivity.
  • Replication fork reversal, mediated by SMARCAL1 and ZRANB3, suppresses these gaps.

Purpose of the Study:

  • Investigate the role of MRNIP in regulating ssDNA gaps during replication stress.
  • Determine MRNIP's function when replication fork reversal is compromised.

Main Methods:

  • Cellular models with perturbed fork reversal (Olaparib treatment, SMARCAL1/ZRANB3 depletion).
  • Analysis of PRIMPOL and MRE11-dependent ssDNA gap prevalence.
  • Assessment of MRNIP-deficient cell sensitivity to PARP inhibition.
  • Investigation of gap-filling mechanisms in MRNIP-deficient cells.

Main Results:

  • MRNIP limits PRIMPOL and MRE11-dependent ssDNA gaps when fork reversal is perturbed.
  • MRNIP-deficient cells exhibit sensitivity to PARP inhibition and accumulate PRIMPOL-dependent DNA damage.
  • UBC13-mediated template switching involving REV1 and Pol-ζ drives gap filling in MRNIP-deficient cells.

Conclusions:

  • MRNIP plays a pro-survival role by regulating post-replicative ssDNA gap dynamics.
  • This study identifies MRNIP as a direct MRE11 regulator modulating ssDNA gap prevalence.