GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE277nnn/GSE277367/primaryOK200Genomics Mus musculusHomo sapiensGenome binding/occupancy profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE277367GEOGSEfalseThe functional antagonism between SIRT2 and MOF regulates cell cycle progression and genome stability [ChIP-seq]The control of G2/M transition is a key event for genome stability as it ensures proper completion of DNA replication and repair before progressing into mitosis. One of the key regulators of G2/M checkpoint is the H4K16Ac-acetyltransferase MOF, which plays a major role in chromatin structure, gene expression, DNA damage and genome stability. Here we show that SIRT2, a member of the sirtuin family of NAD+-dependent deacetylases, antagonizes the role of MOF in G2/M. SIRT2 promotes specific inactivation of MOF through deacetylation and degradation of MOF, which results in re-expression of G2/M cell-cycle genes regulated by MOF. Underscoring the functional relevance of this antagonism, both factors play opposed roles in the deposition of the key mark H4K20me1 during G2/M. Consistently, loss of MOF in wt but not in SIRT2-/- cells induces a genome-wide deregulation of H4K20me1 distribution, which results in a premature loading of condensins. Our studies suggest that the G2/M checkpoint is shaped by the balance between both factors and involves condensing regulation and underscores the role of sirtuins in cell cycle control and genome stability under stress.2026/05/06GSE277367GSM8521150GSM8521139GSM8521128GSM8521129GSM8521137GSM8521148GSM8521149GSM8521127GSM8521138GSM8521146GSM8521135GSM8521147GSM8521136GSM8521144GSM8521133GSM8521134GSM8521145GSM8521142GSM8521131GSM8521132GSM8521143GSM8521140GSM8521141GSM85211301702123227277367 Mus musculusHomo sapiens