The human premature aging syndrome Hutchinson Gilford progeria is caused by a mutational defect in the processing of lamin A, a nuclear matrix protein. In a mouse model of this condition, recruitment of repair proteins to sites of DNA damage is delayed. The molecular mechanism underlying this delayed repair response involves a histone acetylation defect. Specifically, histone H4 is hypoacetylated at a lysine 16 residue (H4K16) and this defect is due to reduced association of histone acetyltransferase, Mof, to the nuclear matrix