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Fig. 6 | Epigenetics & Chromatin

Fig. 6

From: Ethionine-mediated reduction of S-adenosylmethionine is responsible for the neural tube defects in the developing mouse embryo-mediated m6A modification and is involved in neural tube defects via modulating Wnt/β-catenin signaling pathway

Fig. 6

Knockdown of METTL3 and overexpression of ALKBH5 disrupt the balance of cell proliferation and apoptosis. A, B HT-22 cells were treated with wild type (SiNc) and METTL3 knock-out (SiMettl3), and cell cycle distribution was analyzed by flow cytometry. The percentages of cells in cell cycle phases were calculated from three independent experiments. C, D Apoptosis in HT-22 cells was measured and analyzed by flow cytometry. The combined early and late apoptosis rates were up-regulated significantly in the SiMettl3 group compared with those in the SiNc group. E, F The Brdu-positive cell of HT-22 cells from SiMettl3 was lower than that from SiNc.  ∗ ∗∗ p < 0.001 vs SiNc group. G, H Apoptosis in control OE and Alkbh5 OE HT-22 cells was measured and analyzed by flow cytometry. I, J Western blot analysis of the protein levels of total PCNA and Cleaved Caspase-3 in control OE and Alkbh5 OE HT-22 cells. Bar graphs for protein abundance were quantitative data from three independent experiments. β-Tubulin was used as a loading control

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Epigenetics & Chromatin

ISSN: 1756-8935