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Deacetylation Assays to Unravel the Interplay between Sirtuins (SIRT2) and Specific Protein-substrates
Published on: February 27, 2016
Un papel para la desacetilación de la histona H3K18 dependiente de SIRT2 en la infección bacteriana
Haig A Eskandarian1, Francis Impens, Marie-Anne Nahori
1Unité des Interactions Bactéries-Cellules, Institut Pasteur, Paris, France.
Science (New York, N.Y.)
|August 3, 2013
Resumen
Las bacterias patógenas reprograman las células del huésped secuestrando la sirtuina 2 de la desacetilasa (SIRT2). Este mecanismo epigenético implica la desacetilación de histonas mediada por SIRT2, crucial para el éxito de la infección bacteriana.
Área de la Ciencia:
- Microbiología Microbiología.
- La epigenética es la epigenética.
- Biología Molecular Biología Molecular
Sus antecedentes:
- Los patógenos manipulan la transcripción celular del huésped durante la infección.
- Los mecanismos subyacentes a los cambios transcripcionales inducidos por patógenos a menudo no están claros.
Objetivo del estudio:
- Para aclarar el papel de la sirtuina 2 de la desacetilasa del huésped (SIRT2) en la infección por Listeria monocytogenes.
- Investigar los mecanismos epigenéticos empleados por los patógenos para alterar la transcripción del huésped.
Principales métodos:
- Estudió la translocación de SIRT2 al núcleo durante la infección por Listeria monocytogenes.
- Se investigó la asociación de SIRT2 con los sitios de inicio de la transcripción génica.
- Se analizó la histona H3 lisina 18 (H3K18) desacetilación.
- Utilizó la inhibición de la actividad de SIRT2 y el nocaut de SIRT2 (SIRT2-/-) en modelos de ratón.
Principales resultados:
- La infección por Listeria monocytogenes desencadena la translocación nuclear de SIRT2, dependiente del factor bacteriano InlB.
- SIRT2 se asocia con los sitios de inicio de la transcripción de los genes reprimidos durante la infección.
- SIRT2 desacetila el histón H3 en la lisina 18 (H3K18).
- El bloqueo de la actividad de SIRT2 o el uso de SIRT2-/- en ratones perjudica significativamente la infección bacteriana.
Conclusiones:
- La desacetilación de H3K18 mediada por SIRT2 es crítica para la infección por Listeria monocytogenes.
- Las bacterias patógenas utilizan la reprogramación epigenética a través de SIRT2 para controlar las células huésped.
- Este estudio revela un nuevo mecanismo epigenético impuesto por los patógenos.
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