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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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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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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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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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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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The Replisome03:01

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DNA replication is carried out by a large complex of proteins that act in a coordinated matter to achieve high-fidelity DNA replication. Together this complex is known as the DNA replication machinery or the replisome.
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Updated: Aug 20, 2025

Direct Restart of a Replication Fork Stalled by a Head-On RNA Polymerase
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Los multiméricos MYC protegen las horquillas de replicación estancadas de la ARN polimerasa

Daniel Solvie1, Apoorva Baluapuri1,2,3, Leonie Uhl1

  • 1Department of Biochemistry and Molecular Biology, University of Würzburg, Würzburg, Germany.

Nature
|November 24, 2022
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Las oncoproteínas MYC forman estructuras que ayudan a las células cancerosas a sobrevivir al estrés coordinando la reparación y la replicación del ADN, limitando el daño del ADN durante la fase S.

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Área de la Ciencia:

  • Biología molecular
  • Biología del cáncer
  • Respuesta Celular al Estrés

Sus antecedentes:

  • Las oncoproteínas MYC son factores cruciales para el desarrollo de tumores en humanos.
  • Las proteínas MYC regulan la transcripción, la replicación del ADN y la reparación del daño en las células normales.

Objetivo del estudio:

  • Para aclarar los mecanismos detrás de las diversas funciones celulares de MYC.
  • Investigar los cambios estructurales y las consecuencias funcionales de la perturbación MYC.

Principales métodos:

  • Análisis del comportamiento de la proteína MYC tras la perturbación de la elongación de la transcripción, el empalme del ARNm y la inhibición del proteosoma.
  • Caracterización de los cambios en el interactoma MYC y la formación de multimeros.
  • Estudios de localización de los multiméricos MYC en relación con las bifurcaciones de replicación estancadas y las proteínas de reparación del ADN (FANCD2, ATR, BRCA1).

Principales resultados:

  • MYC se disocia de los promotores y forma estructuras multiméricas bajo estrés celular.
  • La multimerización de MYC altera su interactoma hacia la terminación de la transcripción y los factores de procesamiento de ARN.
  • Los multiméricos MYC se acumulan cerca de las horquillas de replicación estancadas, interactuando con las proteínas de reparación del ADN y bloqueando la transcripción antisentido.

Conclusiones:

  • La multimerización MYC es un proceso dependiente de la ubicuidad desencadenado por el estrés celular.
  • Los multiméricos MYC estabilizan las proteínas de reparación del ADN en las bifurcaciones de replicación estancadas, limitando las rupturas de doble hebra del ADN.
  • La multimerización MYC es un mecanismo clave que permite la proliferación de células tumorales en condiciones estresantes.