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Related Concept Videos

The DNA Replication Fork01:02

The DNA Replication Fork

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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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Translesion DNA Polymerases02:10

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Translesion (TLS) polymerases rescue stalled DNA polymerases at sites of damaged bases by replacing the replicative polymerase and installing a nucleotide across the damaged site. Doing so, TLS allows additional time for the cell to repair the damage before resuming regular DNA replication.
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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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Restarting Stalled Replication Forks02:37

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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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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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Replication in Prokaryotes01:32

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DNA replication has three main steps: initiation, elongation, and termination. Replication in prokaryotes begins when initiator proteins bind to the single origin of replication (ori) on the cell's circular chromosome. Replication then proceeds around the entire circle of the chromosome in each direction from the two replication forks, resulting in two DNA molecules.
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Compensatory Evolution to DNA Replication Stress is Robust to Nutrient Availability.

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Evolutionary repair following DNA replication stress is predictable across environments. Recurrent mutations conferring fitness advantages were identified, revealing robust adaptation mechanisms with implications for genome stability and cancer research.

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Area of Science:

  • Evolutionary Biology
  • Genetics
  • Molecular Biology

Background:

  • Evolutionary repair describes compensatory evolution after cellular process disruptions.
  • Genotype-by-environment interactions can shape evolutionary trajectories.
  • DNA replication stress causes genetic instability, impairing DNA synthesis.

Purpose of the Study:

  • To test the predictability of evolutionary repair under DNA replication stress.
  • To investigate the influence of glucose availability on adaptation.
  • To identify genetic mechanisms underlying adaptation to replication stress.

Main Methods:

  • High-throughput experimental evolution of *Saccharomyces cerevisiae* under constitutive replication stress.
  • Growth under varying glucose concentrations to assess environmental impact.
  • Analysis of recurrent mutations and their fitness effects across environments.

Main Results:

  • Glucose levels affected physiology and adaptation rates but not the robustness of adaptation genetics.
  • Recurrent mutations consistently improved fitness across different glucose availabilities.
  • A novel role for the mediator complex of RNA polymerase II in adaptation was discovered.

Conclusions:

  • Evolutionary repair to DNA replication stress is robust and predictable.
  • Adaptation mechanisms are largely independent of macronutrient availability.
  • Findings offer insights into genome stability and potential links to cancer development.