西亚试剂：SIRT1 Redistribution on Chromatin Promotes Genomic Stabilit

SIRT1 Redistribution on Chromatin Promotes Genomic Stability but Alters Gene Expression during Aging

Philipp Oberdoerffer1,Shaday Michan1,Michael McVay1,Raul Mostoslavsky2,James Vann3,Sang-Kyu Park3,Andrea Hartlerode4,Judith Stegmuller1,7,Angela Hafner1,Patrick Loerch1,Sarah M. Wright5,Kevin D. Mills5,Azad Bonni1,Bruce A. Yankner1,Ralph Scully4,Tomas A. Prolla3,Frederick W. Alt6andDavid A. Sinclair1,,

1 Department of Pathology and Glenn Labs for Aging Research, Harvard Medical School, Boston, MA 02115, USA
2 Massachusetts General Hospital Cancer Center, Boston, MA 02114, USA
3 University of Wisconsin, Department of Genetics and Medical Genetics, Madison, WI 53706, USA
4 Department of Medicine, Harvard Medical School and Beth Israel Deaconess Medical Center, Boston, MA 02115, USA
5 The Jackson Laboratory, Bar Harbor, ME 04609, USA
6 Howard Hughes Medical Institute, The Children's Hospital, Immune Disease Institute, and Department of Genetics, Harvard Medical School, Boston, MA 02115, USA
7 Present address: Max Planck Institute for Experimental Medicine, 37075 G?ttingen, Germany

Genomic instability and alterations in gene expression are hallmarks of eukaryotic aging. The yeast histone deacetylase Sir2 silences transcription and stabilizes repetitive DNA, but during aging or in response to a DNA break, the Sir complex relocalizes to sites of genomic instability, resulting in the desilencing of genes that cause sterility, a characteristic of yeast aging. Using embryonic stem cells, we show that mammalian Sir2, SIRT1, represses repetitive DNA and a functionally diverse set of genes across the mouse genome. In response to DNA damage, SIRT1 dissociates from these loci and relocalizes to DNA breaks to promote repair, resulting in transcriptional changes that parallel those in the aging mouse brain. Increased SIRT1 expression promotes survival in a mouse model of genomic instability and suppresses age-dependent transcriptional changes. Thus, DNA damage-induced redistribution of SIRT1 and other chromatin-modifying proteins may be a conserved mechanism of aging in eukaryotes.

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