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SRX757045: GSM1542270: Sample_LSD1_SH-SY5Y_B0_S63; Homo sapiens; ChIP-Seq
1 ILLUMINA (Illumina HiSeq 2500) run: 16.5M spots, 839.2M bases, 507Mb downloads

Submitted by: Gene Expression Omnibus (GEO)
Study: The LSD1/KDM1A neuro-specific isoform regulates neuronal differentiation through H3K9 demethylation [ChIP-Seq]
show Abstracthide Abstract
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. Overall design: Examination of 2 different LSD1 isoforms LSD1 and LSD1+8a, LSD1+8a''s cofactor SVIL, H3K9me2 in SH-SY5Y cells infected with control or LSD1+8a shRNA during neuronal maturation induced with BNDF at Day0(B0) and Day3(B3).ChIP-seq datas were generated by deep sequencer Hiseq2500.
Sample: Sample_LSD1_SH-SY5Y_B0_S63
SAMN03174684 • SRS742242 • All experiments • All runs
Organism: Homo sapiens
Library:
Instrument: Illumina HiSeq 2500
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: SINGLE
Construction protocol: Cells were fixed with 1% formaldehyde for 10 minutes at room temperature before termination with 0.125 M glycine. Cells were then lysed in ChIP buffer (0.6% SDS, 10 mM EDTA, and 50 mM Tris-HCl, pH 8.1) and cross-linked chromatin was sonicated to obtain DNA fragments of 300–800 bp. Immunoprecipitations were performed following the Upstate protocol (http://www.upstate.com). DNA was recovered by phenol-chloroform extraction and ethanol precipitation. ChIP-seq libraries were prepared using NEBNext DNA library preparation reagents (E6000) and the protocol and reagents concentrations described in the Illumina Multiplex ChIP-seq DNA sample Prep Kit. Libraries were indexed using a single indexed PCR primer. After PCR amplification, 300-600 bp DNA fragments were selected on an agarose gel. Libraries were quantified by Qubit (Invitrogen), and library size was assessed by Bioanalyzer (Agilent). Libraries were sequenced using a HiSeq 2000 (Illumina) to generate 50 bp single end reads.
Experiment attributes:
GEO Accession: GSM1542270
Links:
External link:
Runs: 1 run, 16.5M spots, 839.2M bases, 507Mb
Run# of Spots# of BasesSizePublished
SRR164784116,454,030839.2M507Mb2015-07-08

ID:
1093954

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