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Targeting Menin disrupts the KMT2A/B and polycomb balance to paradoxically activate bivalent genes - Nature Cell Biology
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Precise control of activating H3K4me3 and repressive H3K27me3 histone modifications at bivalent promoters is essential for normal development and frequently corrupted in cancer. By coupling a cell surface readout of bivalent MHC class I gene expression with whole-genome CRISPR–Cas9 screens, we identify specific roles for MTF2–PRC2.1, PCGF1–PRC1.1 and Menin–KMT2A/B complexes in maintaining bivalency.
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