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Abstract The prolyl hydroxylase domain-containing proteins (PHD1-3) and the asparaginyl hydroxlyase factor inhibiting HIF (FIH) are oxygen sensors for hypoxia-inducible factor-driven transcription of hypoxia-induced genes, but whether these sensors affect oxygen-dependent epigenetic regulation more broadly is not known. Here, we show that FIH exerts an additional role as an oxygen sensor in epigenetic control by the histone lysine methyltransferases G9a and GLP. FIH hydroxylated and inhibited G9

The N-terminal acetyltransferase A (NatA) complex, which is composed of NAA10 and NAA15, catalyzes N-terminal acetylation of many proteins in a co-translational manner. Structurally, the catalytic subunit NAA10 was believed to have no activity toward an internal lysine residue because the gate of its catalytic pocket is too narrow. However, several studies have demonstrated that the monomeric NAA10 can acetylate the internal lysine residues of several substrates including hypoxia-inducible facto

The development of non-human primate models is essential for the fields of developmental and regenerative biology because those models will more closely approximate human biology than do murine models. Based on single cell RNAseq and fluorescence-activated cell sorting, we report the identification and functional characterization of two quiescent stem cell populations (skeletal muscle stem cells (MuSCs) and mesenchymal stem cells termed fibro-adipogenic progenitors (FAPs)) in the non-human prima

Aging is characterized by a decline in the ability of tissue repair and regeneration after injury. In skeletal muscle, this decline is largely driven by impaired function of muscle stem cells (MuSCs) to efficiently contribute to muscle regeneration. We uncovered a cause of this aging-associated dysfunction: a cellular survivorship bias that prioritizes stem cell persistence at the expense of functionality. With age, MuSCs increased expression of a tumor suppressor, N-myc down-regulated gene 1 (N

<p>The FIH-G9a/GLP axis regulates invasive potential of OvCa cells in an oxygen dependent manner. This file is related to Fig. 4.</p>

<p>Molecular dynamics simulation of H3K9me2 binding to unmodified GLP-ARD. These movies are related to main Fig. 3D.</p>

<p>G9a/GLP mutations recorded in COSMIC database. These data are related to Fig. 6.</p>

<p>The FIH-G9a/GLP axis regulates invasive potential of OvCa cells in an oxygen dependent manner. This file is related to Fig. 4.</p>

<p>FIH hydroxylates G9a/GLP at Asn residues in ARD and inhibits G9a/GLP-mediated gene repression. This file is related to Fig. 2-3.</p>

<p>Sequences of si/shRNAs and PCR primers. Information on cancer tissues. Gene sets correlated with G9a or FIH expression.</p>

<div>Abstract<p>The prolyl hydroxylase domain-containing proteins (PHD1-3) and the asparaginyl hydroxlyase factor inhibiting HIF (FIH) are oxygen sensors for hypoxia-inducible factor-driven transcription of hypoxia-induced genes, but whether these sensors affect oxygen-dependent epigenetic regulation more broadly is not known. Here, we show that FIH exerts an additional role as an oxygen sensor in epigenetic control by the histone lysine methyltransferases G9a and GLP. FIH hydroxylat

<p>FIH hydroxylates G9a/GLP at Asn residues in ARD and inhibits G9a/GLP-mediated gene repression. This file is related to Fig. 2-3.</p>

<p>Histone H3/4 modifications and oxygen-dependent H3K9 methylation by FIH and G9a/GLP. This file is related to Fig. 1.</p>