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Establishment of constitutive heterochromatin in Drosophila early embryos involves H3K14ac-mediated recruitment of Eggless/SetDB1

ABSTRACT: Establishment of constitutive heterochromatin in Drosophila early embryos involves H3K14ac-mediated recruitment of Eggless/SetDB1

PROVIDER: PRJNA1012473 | ENA |

REPOSITORIES: ENA

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Establishment of constitutive heterochromatin in Drosophila early embryos involves H3K14ac-mediated recruitment of Eggless/SetDB1

Project description:The establishment of heterochromatin is a crucial process in the early embryonic development. Recent research suggests that SetDB1 is necessary for heterochromatin establishment in the early embryonic development of Drosophila. Additionally, SetDB1 has been found to bind to H3K14ac in mammalian cells. However, the role of the H3K14ac in heterochromatin establishment during embryogenesis remains unknown. Here we discovered that the active modification H3K14ac serves as an intergenerational marker from oocytes to early embryos, and it is recognized by Eggless/SetDB1 through its Tudor domains. Furthermore, we have introduced a point-mutation in the endogenous Eggless/SetDB1 locus, resulting in the loss of H3K14ac-binding. Both H3K14ac attenuation and SetDB1 mutant embryos exhibit abnormal heterochromatin formation and genomic instability. We reveal a novel model of heterochromatin establishment via H3K14ac-mediated recruitment of SetDB1.

2024-08-06 | GSE242239 | GEO

Hdac3, Setdb1, and Kap1 mark H3K9me3/H3K14ac bivalent regions in young and aged liver.

Project description:Post-translational modifications of histone tails play a crucial role in gene regulation. Here, we performed chromatin profiling by quantitative targeted mass spectrometry to assess all possible modifications of the core histones. We discovered a novel bivalent combination, a dually-marked H3K9me3/H3K14ac modification in the liver, that is significantly decreased in old hepatocytes. Subsequent genome-wide location analysis (ChIP-Seq) identified 1032 and 668 bivalent regions in young and old livers, respectively, with 280 in common. Histone H3K9 deacetylase Hdac3, as well as H3K9 methyltransferase Setdb1, found in complex Kap1, occupied bivalent regions in both young and old livers, correlating to presence of H3K9me3. Expression of genes associated with bivalent regions in young liver, including those regulating cholesterol secretion and triglyceride synthesis, is upregulated in old liver once the bivalency is lost. Hence, H3K9me3/H3K14ac dually-marked regions define a poised inactive state that is resolved with loss of one or both of the chromatin marks, which subsequently leads to change in gene expression.

2019-12-02 | GSE130712 | GEO

H3K14ac is linked to methylation of H3K9 by the Tudor domains of SETDB1

Project description:Mononucleosomes were isolated from murine ES cells and precipitated with the recombinant SETDB1 Triple Tudor Domain (3TD), recombinant SETDB1 Triple Tudor domain Y268A mutant, anti-H3K9me2 (Abcam, ab1220), or anti-H3K9me1 (Abcam, ab8896, Lot GR185298-1) antibodies.

2018-07-30 | E-MTAB-4982 | biostudies-arrayexpress

H3K14ac is linked to methylation of H3K9 by the Tudor domains of SETDB1

Project description:H3K14ac is linked to methylation of H3K9 by the Tudor domains of SETDB1

| PRJEB15097 | ENA

Hdac3, Setdb1, and Kap1 mark H3K9me3/H3K14ac bivalent regions in young and aged liver.

Project description:Hdac3, Setdb1, and Kap1 mark H3K9me3/H3K14ac bivalent regions in young and aged liver.

| PRJNA541069 | ENA

Timecourse gene expression microarray analysis of bi-allelic targeted Setdb1 mutant mouse ES cells, comparing cells with one inducible conditional (floxed) null allele and a second constitutive null allele, to control mouse ES cell lines.

Project description:Gene expression microarray analysis of Setdb1 inducible conditional (floxed) mutant (Setdb1^tm1c(EUCOMM)Wtsi/Setdb1^tm1Wcs) compared to control (Setdb1^tm1c(EUCOMM)Wtsi/+) ES cell lines, without 4'OHT treatment, and timecourse samples following a 48 hour 4'OHT treatment. The 4'OHT induces Cre recombination via the Rosa26CreERT2 knock-in system, to convert the tm1c conditional allele to the tm1d null allele. The Setdb1^tm1Wcs allele is a constitutive null allele. Experimental and control Setdb1 ES cells were each treated with 4’OHT for 48 hours, and gene expression was analyzed at days 0 (before treatment), 2 (end of treatment period), 3, 4, and 6 days. Three biological replicates per genotype per timepoint (individual ES clones) were performed. Parental ES cell lines are from the International Knockout Mouse Consortium (IKMC - EUCOMM and KOMP-CSD programmes) and were modified using bi-allelic gene targeting with a targeted trapping vector generated by re-purposing Intermediate Vectors from the IKMC resource.

2017-09-12 | E-MTAB-5931 | biostudies-arrayexpress

Hypoxia stabilizes SETDB1 to maintain genome stability

Project description:Von Hippel-Lindau (VHL) is a tumor suppressor that functions as the substrate recognition subunit of the CRL2VHL E3 complex. While substrates of VHL have been identified, its tumor suppressive role remains to be fully understood. For further determination of VHL substrates, we analyzed the physical interactome of VHL and identified the histone H3K9 methyltransferase SETBD1 as a novel target. SETDB1 undergoes oxygen-dependent hydroxylation by prolyl hydroxylase domain proteins (PHD) and the CRL2VHL complex recognizes hydroxylated SETDB1 for ubiquitin-mediated degradation. Under hypoxic conditions, SETDB1 accumulates by escaping CRL2VHL activity. Loss of SETDB1 in hypoxia compared with that in normoxia escalates the production of transposable element (TE)-derived double-stranded RNAs (dsRNAs), thereby hyperactivating the immune-inflammatory response. In addition, strong derepression of TEs in hypoxic cells lacking SETDB1 triggers DNA damage-induced death. Our collective results support a molecular mechanism of oxygen-dependent SETDB1 degradation by the CRL2VHL E3 complex and reveal a role of SETDB1 in genome stability under hypoxia.

2024-01-26 | PXD037104 | Pride

Identification of Setdb1 interaction proteins in neural stem cells

Project description:Setdb1 is an epigenetic factors catalyzing modification of H3K9me3. Expression of its gene is localized to embryonic neural cells during vertebrate embryogenesis, suggesting its role in regulating neural stemness. The project is to identify the interaction partners of Setdb1, by which Setdb1 regulates neural stemness in neural stem cells.

2022-08-12 | PXD030453 | Pride

ZMYND8 reads the dual histone mark H3K4me1-H3K14ac to antagonize the expression of metastasis-linked genes

Project description:Histone acetylation, including acetylated H3K14 (H3K14ac), is generally linked to gene activation. Monomethylated histone H3 lysine 4 (H3K4me1), together with other gene-activating marks, denotes active genes. In contrast to usual gene-activating functions of H3K14ac and H3K4me1, we here show that the dual histone modification mark H3K4me1-H3K14ac is recognized by ZMYND8 (also called RACK7) and functions to counteract gene expression. We identified ZMYND8 as a transcriptional corepressor of the H3K4 demethylase JARID1D. ZMYND8 antagonizes the expression of metastasis-linked genes, and its knockdown increases the cellular invasiveness in vitro and in vivo. The plant homeodomain (PHD) and Bromodomain cassette in ZMYND8 mediates the combinatorial recognition of H3K4me1-H3K14ac and H3K4me0-H3K14ac by ZMYND8. These findings uncover an unexpected role for the signature H3K4me1-H3K14ac in attenuating gene expression and reveal a previously unknown metastasis-suppressive epigenetic mechanism in which ZMYND8's PHD-Bromo cassette couples H3K4me1-H3K14ac with repression of metastasis-linked genes. i) ChIP-Seq data of ZMYND8, JARID1D, H3K4me1, H3K14ac, H3K4me3, and H3K27me3 in normal DU145 cells. ii) ChIP-Seq data of H3K4me1 and H3K4me3 in shLuciferase-, shJARID1D-, or shZMYND8-treated DU145 cells. iii) RNA-Seq data in shLuciferase-, shJARID1D-, or shZMYND8-treated DU145 cells.

2016-07-28 | E-GEOD-82260 | biostudies-arrayexpress

ZMYND8 reads the dual histone mark H3K4me1-H3K14ac to antagonize the expression of metastasis-linked genes

2016-07-28 | GSE82260 | GEO