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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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El ATM controla la formación de ruptura meiotica de doble hilo.

Julian Lange1, Jing Pan, Francesca Cole

  • 1Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA.

Nature
|October 18, 2011
PubMed
Resumen

La ATM quinasa restringe la formación de ruptura de doble hebra (DSB) durante la meiosis al suprimir la actividad de SPO11. Este bucle de retroalimentación negativa previene el exceso de DSB, crucial para prevenir los errores meióticos y la disgenesis gonadal.

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Área de la Ciencia:

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

Sus antecedentes:

  • La recombinación meiótica es iniciada por roturas programadas de doble hebra (DSB) formadas por SPO11.
  • La formación adecuada de DSB es esencial para el emparejamiento y la segregación de cromosomas homólogos.
  • Los DSBs excesivos o mal reparados pueden conducir a la detención meiotic o mutaciones.

Objetivo del estudio:

  • Investigar los mecanismos que controlan el número de rupturas meioticas de doble hilo (DSB).
  • Determinar el papel de la ATM quinasa en la regulación de la formación de DSB durante la meiosis.
  • Para dilucidar la base molecular de la disgenesis gonadal en individuos con deficiencia de ATM.

Principales métodos:

  • Análisis de los complejos de oligonucleótidos SPO11 en espermatocitos de ratón de tipo salvaje y con deficiencia de ATM.
  • Manipulación genética de los niveles de la proteína SPO11 en el contexto de la mutación ATM.
  • Investigando la activación de la ATM quinasa en respuesta al daño del ADN.

Principales resultados:

  • Los espermatocitos que carecen de ATM exhiben un aumento de diez veces en los complejos de oligonucleótidos SPO11, lo que indica una formación elevada de DSB.
  • La deficiencia de ATM hace que los niveles de oligonucleótido SPO11 sean sensibles a los cambios en los niveles de proteína SPO11.
  • La activación de la ATM quinasa por parte de las DSB parece suprimir la formación de nuevas DSB.

Conclusiones:

  • ATM actúa como un regulador negativo de la formación de DSB meiotic a través de un bucle de retroalimentación.
  • Este control de los DSB mediado por ATM es esencial para prevenir rupturas excesivas del ADN y garantizar una meiosis adecuada.
  • Los hallazgos proporcionan una explicación molecular para la disgenesis gonadal en pacientes con ataxia telangiectasia.