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LSD1/KDM1A Maintains Genome-wide Homeostasis of Transcriptional Enhancers [ChIP-Seq]

ABSTRACT: We performed ChIP-Seq in Lsd1-WT, Lsd1-GT and Kdm5c-WT mouse embryonic stem cells (mES).

ORGANISM(S): Mus musculus

PROVIDER: GSE94552 | GEO | 2020/09/01

REPOSITORIES: GEO

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LSD1/KDM1A Maintains Genome-wide Homeostasis of Transcriptional Enhancers [RNA-Seq]

Project description:We performed sequencing of Nuclear RNA from Lsd1-WT, Lsd1-GT, KDM5c-WT, and KDM5C-KO mouse embryonic stem cells (mES). We also performed sequencing of Total RNA from Lsd1-WT and Lsd1-GT mES.

2020-09-01 | GSE94556 | GEO

LSD1/KDM1A Maintains Genome-wide Homeostasis of Transcriptional Enhancers [GRO-Seq]

Project description:We performed GRO-Seq in Lsd1-WT and Lsd1-GT mouse embryonic stem cells (mES).SMCX_WT (KDM5c_WT) and SMCX_KO (KDM5c_KO) represent two additional mES cell lines used in the GRO-Seq study.

2020-09-01 | GSE93951 | GEO

LSD1/KDM1A Maintains Genome-wide Homeostasis of Transcriptional Enhancers [BrU-Seq]

Project description:We performed BrU-Seq after shRNA mediated depletion of Lsd1 in primary cultures of mouse cortical neurons.

2020-09-01 | GSE93938 | GEO

KDM1A maintains genome-wide homeostasis of transcriptional enhancers.

Project description: Not available

| S-EPMC7849409 | biostudies-literature

LSD1/KDM1A Maintains Genome-wide Homeostasis of Transcriptional Enhancers

Project description:LSD1/KDM1A Maintains Genome-wide Homeostasis of Transcriptional Enhancers

| PRJNA362885 | ENA

LSD1/KDM1A Maintains Genome-wide Homeostasis of Transcriptional Enhancers

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-09-01 | GSE93952 | GEO

GR and LSD1/KDM1A-Targeted Gene Activation Requires Selective H3K4me2 Demethylation at Enhancers.

Project description: Not available

| S-EPMC7433711 | biostudies-literature

The LSD1/KDM1A neuro-specific isoform regulates neuronal differentiation through H3K9 demethylation [Affymetrix]

Project description:During brain development, histone-modifying enzymes play an important role by orchestrating transcriptional programs that regulate neuronal maturation. Lysine-Specific Demethylase 1 (LSD1, also named as KDM1A) functions as a transcriptional repressor by removing methyl groups at lysine 4 of histone H3 (H3K4). In neurons, alternative splicing can include an additional exon (exon E8a) within LSD1 transcripts, generating a LSD1+8a neuro-specific isoform. We here report that LSD1+8a isoform does not have the intrinsic ability to demethylate H3K4. LSD1+8a functions as a co-activator on its target genes by removing H3K9 repressive histone marks. We identify the supervillin protein (SVIL) as a LSD1+8a interacting partner and demonstrate that SVIL protein regulates neuronal maturation by controlling LSD1+8a mediated H3K9 demethylation. Thus, our results show that alternative splicing provides a genius mechanism by which LSD1 isoforms can acquire a dual specificity (H3K9 vs H3K4) and therefore differentially control specific gene expression patterns during brain development. In order to find some LSD1+8a regulated genes at differentiated SH-SY5Y cell lines, we infected SH-SY5Y with control or LSD1+8a shRNA, then induced differentiation with RA and BDNF, (Retinoic acid (RA) (Sigma) was added at a final concentration of 10 μM the next day after plating. After 4 days, the cells were washed three times with PBS and incubated with 50 ng/mL of Brain Derived Neural Factor (BDNF) (Millipore) in serum-free medium for 3 days), we extracted RNA from BDNF induced SH-SY5Y cells for expression analysis.Duplicates were included for Affymetrix Human transcriptome version 2 array.

2015-06-05 | E-GEOD-63097 | biostudies-arrayexpress

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [ChIP-seq]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. ChIP-seq with Scl, Hand1, Lsd1, Ezh2, H3K4me1 and H3K27ac in different cell types with mesodermal origin. Scl ChIP-seq in WT, SclKO, SclKO-iScl and Gata12KO mES cell derived day4 EB (embryoid body) Flk1+ mesodermal cells, SclKO-iScl ES cells and MEL cells; Hand1 ChIP-seq in WT mES cell derived day4 EB Flk1+ mesodermal cells; Lsd1 and Ezh2 ChIP-seq in WT and SclKO mES cell derived day4 EB Flk1+ mesodermal cells. ChIP-seq of histone modifications H3K4me1 and H3K27ac in WT, SclKO and Gata12KO mES cell derived day4 EB Flk1+ mesodermal cells, HPC7 hematopoietic progenitor cells and HL1 cardiomyogenic cells

2015-01-01 | E-GEOD-47082 | biostudies-arrayexpress

Targeting the scaffolding role of LSD1 (KDM1A) poises acute myeloid leukemia cells for Retinoic Acid induced differentiation

Project description:The histone demethylase LSD1 is deregulated in several tumors, including leukemias, providing the rationale for the clinical use of LSD1 inhibitors. In acute promyelocytic leukemia (APL), pharmacological doses of retinoic acid (RA) induce differentiation of APL cells through degradation of the PML-RAR oncogene. APL cells are resistant to LSD1 inhibition or knock-out, but LSD1 inhibition sensitizes them to physiological doses of RA without altering the stability of PML-RAR, and extends survival of leukemic mice upon RA treatment. Non-enzymatic activities of LSD1 are essential to block differentiation of leukemic cells, while the combination of LSD1 inhibitors (or LSD1 knock-out) with low doses of RA releases a differentiation-associated gene expression program, not strictly dependent on changes in histone H3K4 methylation (known substrate of LSD1). An integrated proteomic/epigenomic/mutational analysis showed that LSD1 inhibitors alter the recruitment of LSD1-containing complexes to chromatin through inhibition of the interaction between LSD1 and GFI1, a relevant transcription factor in hematopoiesis.

2020-05-26 | PXD012954 | Pride

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