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The functional antagonism between SIRT2 and MOF regulates mitotic entry - PLK1 methylation

ABSTRACT: Mitosis entry is tightly regulated by a complex network of interconnected mechanisms involving epigenetic modifications, signaling pathways, transcriptional control, and structural changes. While significant progress has been made in understanding these processes individually, the mechanisms integrating chromatin dynamics with key mitotic regulators are still not fully understood. Here, we identify a functional antagonism between the deacetylase SIRT2 and the acetyltransferase MOF in the G2/M transition and mitotic progression. This interplay, which involves MOF deacetylation by SIRT2, regulates key histone marks, including H4K16ac deacetylation and H4K20me1 deposition, condensin II loading, the stability of the key mitotic regulator PLK1 and has a major impact on the transcription control of mitosis regulated by the FOXM1. Our findings reveal a previously unrecognized layer of regulation in G2/M progression, shedding light on the intricate crosstalk between chromatin dynamics and mitotic control, with potential implications for understanding chromosomal stability and cancer.

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ORGANISM(S): Homo Sapiens (human)

SUBMITTER: Joan Josep Bech-Serra

LAB HEAD: Alex Vaquero

PROVIDER: PXD065218 | Pride | 2026-04-29

REPOSITORIES: Pride

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Project description:Javasky E, Shamir I, Gandhi S, Egri S, Sandler O, Rothbart SB, Kaplan N, Jaffe JD, Goren A, and Simon I. Genome Research 2018. Mitosis encompasses key molecular changes including chromatin condensation, nuclear envelope breakdown and reduced transcription levels. Immediately after mitosis, the interphase chromatin structure is reestablished and transcription resumes. The reestablishment of the interphase chromatin requires bookmarking, i.e., the retention of at least partial information during mitosis. Yet, while recent studies demonstrate that chromatin accessibility is generally preserved during mitosis and is only locally modulated, the exact details of the bookmarking process and its components are still unclear. To gain a deeper understanding of the mitotic bookmarking process, we merged proteomics, immunofluorescence, and ChIP-seq approaches to study the mitotic and interphase organization in human cells. We focused on key histone modifications, and employed the HeLa-S3 cells as a model system. Generally, we observed a global concordance between the genomic organization of histone modifications in interphase and mitosis, yet the abundance of the two types of modifications we investigated was different. Whereas histone methylation patterns remain highly similar, histone acetylation patterns show a general reduction while maintaining their genomic organization. In line with a recent study demonstrating that minimal transcription is retained during mitosis, we show that RNA polymerase II does not fully disassociate from the genome, but rather maintains its genomic localization at reduced levels. Next, we followed up on previous studies demonstrating that nucleosome depleted regions (NDRs) become occupied by a nucleosome during mitosis. Surprisingly, we observed that the nucleosome introduced into the NDR during mitosis encompasses a distinctive set of histone modifications, differentiating it from the surrounding nucleosomes. We show that the nucleosomes in the vicinity of the NDR appear to both shift into the NDR during mitosis and undergo deacetylation. HDAC inhibition by the small molecule TSA reverts the deacetylation pattern of the shifted nucleosome. Taken together, our results demonstrate that the epigenomic landscape can serve as a major component of the mitotic bookmarking process, and provide evidence for a mitotic deposition and deacetylation of the nucleosomes surrounding the NDR.

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The functional antagonism between SIRT2 and MOF regulates mitotic entry - PLK1 methylation

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