Kmt2c restricts G-CSF-driven HSC mobilization and granulocyte production in a methyltransferase-independent manner.

Gene set enrichment analysis (GSEA) showed highly significant downregulation of interferon-α target genes and other inflammatory pathways in G-CSF-treated Kmt2c Δ/Δ HSCs and other progenitors ( Figures 4D and S6 ), consistent with our prior studies showing that Kmt2c potentiates inflammatory signaling in HSCs. 31 However, inactivating the interferon-α receptor gene Ifnar1 did not hypersensitize HSC/MPPs to G-CSF, suggesting that Kmt2c deletion accelerates HSC mobilization via alternative mechanisms ( Figures S7A – S7H ).

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