Sirt6 Promotes DNA End Joining in iPSCs Derived from Old Mice

Cell Rep. 2017 Mar 21;18(12):2880-2892. doi: 10.1016/j.celrep.2017.02.082.

Abstract

Induced pluripotent stem cells (iPSCs) have great potential for treating age-related diseases, but the genome integrity of iPSCs is critically important. Here, we demonstrate that non-homologous end joining (NHEJ), rather than homologous recombination (HR), is less efficient in iPSCs from old mice than young mice. We further find that Sirt6 is downregulated in iPSCs from old mice. Sirt6 directly binds to Ku80 and facilitates the Ku80/DNA-PKcs interaction, thus promoting DNA-PKcs phosphorylation at residue S2056, leading to efficient NHEJ. Rescue experiments show that introducing a combination of Sirt6 and the Yamanaka factors during reprogramming significantly promotes DNA double-strand break (DSB) repair by activating NHEJ in iPSCs derived from old mice. Thus, our study suggests a strategy to improve the quality of iPSCs derived from old donors by activating NHEJ and stabilizing the genome.

Keywords: Ku80; NHEJ repair; SirT6.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aging / metabolism*
  • Animals
  • Cellular Reprogramming
  • DNA End-Joining Repair*
  • DNA-Activated Protein Kinase
  • DNA-Binding Proteins
  • Fibroblasts / metabolism
  • Genomic Instability
  • Induced Pluripotent Stem Cells / metabolism*
  • Ku Autoantigen / metabolism
  • Mice, Inbred C57BL
  • Nuclear Proteins
  • Phosphorylation
  • Phosphoserine / metabolism
  • Protein Binding
  • Sirtuins / metabolism*
  • Skin / cytology

Substances

  • DNA-Binding Proteins
  • Nuclear Proteins
  • Phosphoserine
  • Sirt6 protein, mouse
  • DNA-Activated Protein Kinase
  • Prkdc protein, mouse
  • Sirtuins
  • Ku Autoantigen