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Related Concept Videos

Genome Copying Errors02:46

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DNA replication is a well-evolved process that copies millions of base pairs with high fidelity during each cell division. Occasionally a wrong base or a long stretch of wrong bases may get added to the daughter strands. If the errors are left unchecked, cells might accumulate several mutations that might endanger their  survival. Therefore, the copying errors are checked and repaired at three levels.
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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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Before a cell can divide, it must accurately replicate all of its chromosomes, including the DNA and its associated histone and non-histone proteins.  This process begins at numerous origins of replication during the S phase of the cell cycle in each of a cell’s chromosomes simultaneously. Certain nucleotides can act as origins of replication, but these sequences are not well defined - especially in complex, multi-cellular, eukaryotic species. The length of DNA that spans an origin...
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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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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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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: Sep 14, 2025

G2-seq: A High Throughput Sequencing-based Technique for Identifying Late Replicating Regions of the Genome
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Evidence that transient replication errors initiate nuclear genome mutations.

Scott A Lujan1, Zhi-Xiong Zhou1, Thomas A Kunkel1

  • 1Laboratory of Genome Stability and Structural Biology, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC 27709, United States.

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This summary is machine-generated.

DNA replication can cause mutations through mismatches and strand slippage. New research shows transient initiator mutagenesis pathways increase mutation rates with longer DNA sequences in yeast, suggesting a universal replication feature.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Genomics

Background:

  • DNA replication is essential for cell division but can introduce errors leading to mutations.
  • Point mutations arise from base-base mismatches (substitutions) or polymerase slippage (indels).
  • In vitro studies suggested transient DNA intermediates contribute to mutations.

Purpose of the Study:

  • To investigate the in vivo role of transient intermediates in DNA mutation.
  • To determine if DNA replication intermediates influence mutation rates in vivo.
  • To explore the relationship between DNA sequence characteristics and mutation frequency.

Main Methods:

  • In vivo studies in the yeast nuclear genome.
  • Analysis of mutation rates at mononucleotide runs of varying lengths.
  • Investigating specific single-base mutations at the 3'-terminus of primer strands.

Main Results:

  • Mutation rates for specific single-base changes increased with the length of mononucleotide runs.
  • Evidence supports the role of transient intermediates in initiating mutations in vivo.
  • Four transient initiator mutagenesis (TIM) pathways were proposed to be active in yeast.

Conclusions:

  • Transient initiator mutagenesis pathways are active during yeast genome replication.
  • The length of mononucleotide runs influences mutation rates in vivo.
  • These TIM pathways may represent a universal mechanism in DNA replication across organisms.