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Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Base Excision Repair01:54

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One of the common DNA damages is the chemical alteration of single bases by alkylation, oxidation, or deamination. The altered bases cause mispairing and strand breakage during replication. This type of damage causes minimal change to the DNA double helix structure and can be repaired by the base excision repair (BER) pathways. BER corrects damaged DNA sequences by removing the damaged base and restoring the original base sequence using the complementary strand as a template.
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The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...
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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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Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1
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Published on: February 17, 2011

Efecto del daño del ADN en un complejo BRCA1

F Wu-Baer1, R Baer

  • 1Institute of Cancer Genetics and Department of Pathology, Columbia University College of Physicians and Surgeons, 1150 St Nicholas Avenue, New York, New York 10032, USA.

Nature
|November 2, 2001
PubMed
Resumen

El complejo BRCA1-CtIP permanece estable después del daño del ADN, al contrario de los hallazgos anteriores. La fosforilación de CtIP por la ATM quinasa no interrumpe esta interacción, lo que afecta a la transcripción del gen de respuesta al daño en el ADN.

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Área de la Ciencia:

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

Sus antecedentes:

  • La proteína supresora del tumor BRCA1 interactúa con CtIP, un sustrato de la ATM quinasa.
  • Estudios anteriores sugirieron que el estrés genotóxico interrumpe la interacción BRCA1-CtIP a través de la fosforilación de CtIP.

Objetivo del estudio:

  • Investigar el efecto de la radiación ionizante y la fosforilación mediada por ATM quinasa en la estabilidad del complejo BRCA1-CtIP.
  • Para determinar si la interrupción del complejo BRCA1-CtIP media la transcripción de los genes de respuesta al daño del ADN.

Principales métodos:

  • Investigó la estabilidad del complejo BRCA1-CtIP en células irradiadas.
  • Se analizó la interacción de las isoformas CtIP fosforiladas con BRCA1 in vivo.
  • Se ha mapeado el dominio de unión al BRCA1 de CtIP en relación con los sitios de fosforilación ATM.

Principales resultados:

  • El complejo BRCA1-CtIP permanece estable en las células expuestas a radiación ionizante.
  • La fosforilación de CtIP por ATM quinasa no impide su interacción in vivo con BRCA1.1.
  • El dominio de unión a BRCA1 de CtIP es distinto de los sitios de fosforilación ATM.

Conclusiones:

  • La interrupción del complejo BRCA1-CtIP no es el mecanismo por el cual los genes de respuesta al daño del ADN se inducen después del estrés genotóxico.
  • Los hallazgos desafían el modelo propuesto por Li et al. con respecto a la disociación del complejo BRCA1-CtIP y la regulación génica.