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DNA Damage can Stall the Cell Cycle02:36

DNA Damage can Stall the Cell Cycle

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...
DNA Damage Can Stall the Cell Cycle02:36

DNA Damage Can Stall the Cell Cycle

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...
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, a...
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The cell cycle is a series of events leading to DNA duplication followed by the division of cell content to form two daughter cells. The cell cycle progresses in four stages—the cell increases in size (gap 1 or G1-phase), duplicates its DNA (synthesis or S-phase), prepares to divide (gap 2 or G2-phase), and divides (mitosis or M-phase).
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S-Cdk Initiates DNA Replication02:38

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Preparation of Meiotic Chromosome Spreads from Mouse Oocytes for Assessment of Synapsis and Recombination
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El inicio de la anafase antes de la replicación completa del ADN con respuestas intactas al punto de control.

Jordi Torres-Rosell1, Giacomo De Piccoli, Violeta Cordon-Preciado

  • 1Cell Cycle Group, Medical Research Council (MRC) Clinical Sciences Centre, Faculty of Medicine, Imperial College London, Hammersmith Hospital Campus, Du Cane Road, London W12 0NN, UK.

Science (New York, N.Y.)
|March 10, 2007
PubMed
Resumen

Los puntos de control celulares previenen la mitosis con horquillas de replicación de ADN estancadas. Sin embargo, este estudio muestra que el complejo Smc5-Smc6 es crucial para completar la replicación antes de la división celular, independientemente de los puntos de control conocidos.

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Área de la Ciencia:

  • Biología celular Biología celular.
  • Biología Molecular Biología Molecular
  • Genética La genética.

Sus antecedentes:

  • Los puntos de control celulares normalmente detienen la mitosis si la replicación del ADN se encuentra en un estancamiento.
  • Se desconoce si los puntos de control aseguran la finalización de la replicación del ADN antes de la mitosis.

Objetivo del estudio:

  • Para investigar si la finalización de la replicación del ADN es monitoreada por puntos de control celulares antes de la mitosis.
  • Comprender el papel del complejo Smc5-Smc6 en la replicación y división celular.

Principales métodos:

  • Utilizado levadura smc5-smc6 mutantes para estudiar la replicación del ADN y la mitosis.
  • Se analizó el tiempo de replicación en los loci naturales que impiden la replicación, incluido el grupo de genes de ADN ribosomal.
  • Se investigó la segregación cromosómica en ausencia de Smc5-Smc6.6 funcional.

Principales resultados:

  • La replicación se retrasó significativamente en los mutantes smc5-smc6, particularmente en el locus del ADN ribosomal.
  • La entrada mitótica ocurrió con una replicación inacabada en los mutantes smc5-smc6, lo que condujo a la no disyunción cromosómica.
  • La eliminación de los obstáculos de la horquilla de replicación en los mutantes smc5-smc6 restauró el acoplamiento temporal entre la replicación y la segregación.

Conclusiones:

  • El complejo Smc5-Smc6 es esencial para la finalización oportuna de la replicación del ADN antes de la mitosis.
  • Los puntos de control celulares conocidos no parecen vigilar la finalización de la replicación del ADN.
  • La finalización de la replicación y la segregación cromosómica se desacoplan temporalmente en los mutantes smc5-smc6 que carecen de Smc5-Smc6.6 funcional.