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Related Concept Videos

The DNA Replication Fork01:02

The DNA Replication Fork

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 forks, one in...
Restarting Stalled Replication Forks02:37

Restarting Stalled Replication Forks

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, a...
Homologous Recombination02:31

Homologous Recombination

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...
Mismatch Repair01:20

Mismatch Repair

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.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
Mismatch Repair01:36

Mismatch Repair

Overview
Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).

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Updated: May 20, 2026

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51
06:24

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51

Published on: February 13, 2019

RAD51 mutants cause replication defects and chromosomal instability.

Tae Moon Kim1, Jun Ho Ko, Lingchuan Hu

  • 1Department of Molecular Medicine and Institute of Biotechnology, University of Texas Health Science Center, San Antonio, Texas, USA.

Molecular and Cellular Biology
|July 11, 2012
PubMed
Summary
This summary is machine-generated.

ATP binding and hydrolysis are essential for RAD51 protein function in DNA repair. Mutant RAD51 proteins disrupt chromosomal maintenance, leading to rearrangements and sensitivity to genotoxins.

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Last Updated: May 20, 2026

Real-time Observation of the DNA Strand Exchange Reaction Mediated by Rad51
06:24

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Published on: February 13, 2019

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • RAD51 protein is crucial for DNA repair pathways, including homology-directed repair (HDR), and restarting stalled replication forks.
  • Studying RAD51 mutants is challenging due to their toxicity, hindering analysis of their specific functions.

Purpose of the Study:

  • To investigate the dominant effects of human RAD51 mutants (defective in ATP binding or hydrolysis) on DNA repair and chromosomal stability in mouse embryonic stem cells.
  • To determine the role of ATP binding and hydrolysis in RAD51's function for chromosomal maintenance.

Main Methods:

  • Expression of dominant human RAD51 mutants (K133A, K133R) in mouse embryonic stem cells also expressing normal mouse RAD51.
  • Assessment of DNA repair capacity, sensitivity to camptothecin, and analysis of chromosomal aberrations.
  • Visualization of RAD51 protein localization using enhanced green fluorescent protein (eGFP) tagging.

Main Results:

  • Cells expressing RAD51 mutants showed defects in restarting stalled replication forks and repairing DNA double-strand breaks (DSBs).
  • These cells exhibited hypersensitivity to camptothecin and a high frequency of structural chromosomal changes, including multiple breakpoints.
  • Mutant RAD51 proteins were found at very low levels at replication and repair sites compared to normal RAD51.

Conclusions:

  • ATP binding and hydrolysis by RAD51 are essential for maintaining chromosomal integrity.
  • Even low levels of non-functional RAD51 mutants can disrupt normal RAD51 activity, leading to genomic instability and chromosomal rearrangements.