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Article Abstract
-methyladenosine (mA) modification plays a critical role in cell cycle regulation, while the mechanism of mA in regulating mitosis remains underexplored. Here, we found that the total mA modification level in cells increased during mitosis by the liquid chromatography-mass spectrometry/mass spectrometry and mA dot blot assays. Silencing methyltransferase-like 3 (METTL3) or METTL14 results in delayed mitosis, abnormal spindle assembly, and chromosome segregation defects by the immunofluorescence. By analyzing transcriptome-wide mA targets in HeLa cells, we identified () as a key gene modified by mA in regulating mitosis. Specifically, through immunoblotting and RNA pulldown, mA modification inhibits PLK1 translation YTH -methyladenosine RNA binding protein 1, thus mediating cell cycle homeostasis. Demethylation of mRNA leads to significant mitotic abnormalities. These findings highlight the critical role of mA in regulating mitosis and the potential of mA as a therapeutic target in proliferative diseases such as cancer.
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