Examining the molecular mechanism behind neuronal genomic stability, Dobbin et al. show that the histone lysine deacetylases HDAC1 and SIRT1 are recruited to the sites of DNA double-strand breaks in neurons and demonstrate the importance of HDAC1-SIRT1 functional interactions in DNA double strand–break repairs. The authors also show that pharmacological activation of SIRT1 can stimulate HDAC1 activity and confer neuroprotection after DNA damage in cultured neurons and in two mouse models of neurodegeneration.
- Matthew M Dobbin
- Ram Madabhushi
- Li-Huei Tsai
