Lamin B1 acetylation slows the G1 to S cell cycle transition through inhibition of DNA repair

Emerging evidence points to post translational modification (PTM) of nuclear lamins as a key regulator of their diverse roles in nuclear organization, chromatin stability, DNA repair, and cell cycle progression. However, the functions of many of these PTMs remain uncharacterized. Here, we demonstrate a role for acetylation at lysine 134 on lamin B1 in slowing the G1 to S cell cycle transition by inhibiting resolution of DNA damage by canonical nonhomologous end joining.