GEO series
The functional antagonism between SIRT2 and MOF regulates cell cycle progression and genome stability [ChIP-seq]
GSE277367
Homo sapiens; Mus musculus
Genome binding/occupancy profiling by high throughput sequencing
24 samples
Submitted 2026/05/06
Platform GPL17021Platform GPL23227
Summary
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.
Published in
Espinosa-Alcantud M, Sima N, Fernández-Duran I et al.
· Science advances 2026
· PMID 42319919
· doi:10.1126/sciadv.aeb2915
This dataset
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Direct links to NCBI, no account and no request form: the whole study as GSE277367_RAW.tar, processed values as the series matrix, the supplementary file directory, and per-sample supplementary files for any of the 24 samples. Raw sequencing reads are also available from ENA.
Also filed as BioProject PRJNA1162051 and SRA study SRP533137. Searching any of these in the dataset finder brings you back here.
Study design
8 conditions, mostly in triplicate
HeLa_WT_H4K20Me1 ×3
HeLa_Kmut_H4K20Me1 ×3
HeLa_WT_INPUT ×3
HeLa_Kmut_INPUT ×3
MEFs_WT_H4K20Me1 ×3
MEFs_MOFKO_H4K20Me1 ×3
MEFs_WT_INPUT ×3
MEFs_MOFKO_INPUT ×3
Supports a between-group comparison across 24 samples.
8 replicated groups read from 24 sample titles; they account for 24 of them. Check it against the sample list below before relying on it.
Samples in this study
0 selected
- GSM8521127 HeLa_WT_H4K20Me1_Rep1
- GSM8521128 HeLa_WT_H4K20Me1_Rep2
- GSM8521129 HeLa_WT_H4K20Me1_Rep3
- GSM8521130 HeLa_Kmut_H4K20Me1_Rep1
- GSM8521131 HeLa_Kmut_H4K20Me1_Rep2
- GSM8521132 HeLa_Kmut_H4K20Me1_Rep3
- GSM8521133 HeLa_WT_INPUT_Rep1
- GSM8521134 HeLa_WT_INPUT_Rep2
- GSM8521135 HeLa_WT_INPUT_Rep3
- GSM8521136 HeLa_Kmut_INPUT_Rep1
- GSM8521137 HeLa_Kmut_INPUT_Rep2
- GSM8521138 HeLa_Kmut_INPUT_Rep3
- GSM8521139 MEFs_WT_H4K20Me1_Rep1
- GSM8521140 MEFs_WT_H4K20Me1_Rep2
- GSM8521141 MEFs_WT_H4K20Me1_Rep3
- GSM8521142 MEFs_MOFKO_H4K20Me1_Rep1
- GSM8521143 MEFs_MOFKO_H4K20Me1_Rep2
- GSM8521144 MEFs_MOFKO_H4K20Me1_Rep3
- GSM8521145 MEFs_WT_INPUT_Rep1
- GSM8521146 MEFs_WT_INPUT_Rep2
- GSM8521147 MEFs_WT_INPUT_Rep3
- GSM8521148 MEFs_MOFKO_INPUT_Rep1
- GSM8521149 MEFs_MOFKO_INPUT_Rep2
- GSM8521150 MEFs_MOFKO_INPUT_Rep3
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