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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 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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The DNA Replication Fork01:02

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Video Experimental Relacionado

Updated: Feb 22, 2026

Author Spotlight: Unveiling the Role of SNF2L in Replication Fork Stability and Genome Duplication
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Author Spotlight: Unveiling the Role of SNF2L in Replication Fork Stability and Genome Duplication

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El complejo RAD51C-XRCC3 regula la resolución de R-loops mediada por FANCM para proteger la integridad del genoma

Satyaranjan Sahoo1, Tarun Nagraj1, Debanjali Bhattacharya1

  • 1Department of Biochemistry, Indian Institute of Science, Bangalore 560012, India.

Science advances
|February 20, 2026
PubMed
Resumen
Este resumen es generado por máquina.

El complejo RAD51C-XRCC3 previene la inestabilidad genómica resolviendo los R-loops, una estructura de ADN implicada en la anemia de Fanconi (FA). Este complejo interactúa con FANCM para gestionar los R-loops durante el estrés de replicación.

Palabras clave:
anemia de Fanconiintegridad del genomaresolución de R-loopsestrés de replicacióncomplejo RAD51C-XRCC3FANCM

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Área de la Ciencia:

  • Biología Molecular
  • Genética
  • Reparación del ADN

Sus antecedentes:

  • La anemia de Fanconi (FA) es un trastorno genético raro que causa insuficiencia de la médula ósea, defectos de nacimiento y susceptibilidad al cáncer.
  • Las mutaciones en los paralogos de RAD51 se han relacionado con afecciones similares a la FA y cánceres, con funciones conocidas en la reparación del ADN pero funciones poco claras durante el estrés de replicación.

Objetivo del estudio:

  • Investigar el papel de los paralogos de RAD51, específicamente el complejo RAD51C-XRCC3 (CX3), en la vía de la anemia de Fanconi y la respuesta al estrés de replicación.
  • Elucidar el mecanismo por el cual el complejo CX3 influye en el procesamiento de R-loops y la estabilidad genómica.

Principales métodos:

  • Se investigó la interacción entre el complejo CX3 y FANCM.
  • Se evaluó el impacto de la función del complejo CX3 y un mutante patológico (RAD51C R258H) en la resolución de R-loops y la inestabilidad genómica.
  • Se examinó el papel del complejo CX3 en las colisiones transcripción-replicación (TRC).

Principales resultados:

  • El complejo CX3 suprime los R-loops, las colisiones transcripción-replicación (TRC) y la inestabilidad genómica en condiciones fisiológicas y de estrés de replicación.
  • El complejo CX3 interactúa físicamente con FANCM, promoviendo su reclutamiento a sitios de R-loop para su resolución.
  • Un mutante patológico de RAD51C altera la interacción con FANCM y el procesamiento de R-loops, lo que conduce a inestabilidad genómica.

Conclusiones:

  • El complejo CX3 desempeña un papel crucial en la vía de la anemia de Fanconi al mediar la tolerancia a los R-loops.
  • El complejo CX3 previene la inestabilidad genómica inducida por R-loops a través de la resolución de R-loops dependiente de FANCM, independientemente de su papel en el mantenimiento de la horquilla.