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SRX3979871: GSM3106288: EC-EA-3702-INPUT_DAY9; Mus musculus; ChIP-Seq
1 ILLUMINA (Illumina HiSeq 2500) run: 34.5M spots, 1.8G bases, 869.4Mb downloads

Submitted by: NCBI (GEO)
Study: KLF4 binding is involved in the organization and regulation of 3D enhancer networks during acquisition and maintenance of pluripotency [ChIP-seq]
show Abstracthide Abstract
Summary: Cell fate transitions are accompanied by global transcriptional, epigenetic and topological changes driven by transcription factors (TFs), as is strikingly exemplified in somatic cell reprogramming to pluripotent stem cells (PSCs) by OCT4, KLF4, SOX2 and cMYC. How TFs orchestrate the complex molecular changes around their targets in a temporal manner remains largely elusive. Here, using KLF4 as a paradigm, we provide the first TF-centric view of chromatin reorganization and the association to 3D enhancer rewiring and the transcriptional changes of linked genes during reprogramming of mouse embryonic fibroblasts to (MEFs) to PSCs. Inducible depletion of KLF factors in PSC caused a genome-wide decrease in connectivity of enhancers and disruption of KLF4 binding site from PSC-specific enhancers was sufficient to reduce expression of genes within the enhancer hub partly by impairing long-range contacts. Our study provides an integrative view of the intricate activities of a master regulator during a controlled cell fate transition and offers novel insights into the order and nature of molecular events that follow TF binding. Purpose: We captured on a genome-wide scale the binding of KLF4 during iPSC formation and its effects on chromatin state, transcriptional activity and chromatin topology around its targets. Methods: We used a well-characterized reprogramming system to apply genome-wide assays that map KLF4 binding (ChIP-seq), chromatin accessibility (ATAC-seq), enhancer and gene activity (H3K27ac ChIP-seq and RNA-seq), enhancer connectivity (H3K27ac Hi-ChIP) as well as KLF4-centric chromatin looping (KLF4 Hi-ChIP) at different stages during acquisition of pluripotency. Results: Integrative analysis of our results generated a reference map of stage-specific chromatin changes around KLF4 bound loci and established strong links with enhancer. rewiring and concordant transcriptional changes. Genetic manipulation of KLF4 binding from a PSC enhancer further supported the ability of KLF4 to function both as a transcriptional regulator and a chromatin organizer. Conclusions: Our study offers novel insights into the intricate roles of a master regulator during cell fate transition. Overall design: Mouse embryonic fibroblasts (MEFs) (Rosa26-M2rtTA/Col1a1-OKSM) induced with doxycycline (dox) in the presence of ascorbic acid. We collected bulk populations on day 3 after dox treatment, whereas at later stages, on day 6 and day 9, we sorted SSEA1 positive cells to enrich for cells on the trajectory towards induced pluripotency. Finally, we used pluripotent stem cells (PSCs) inclusive of embryonic stem cells (ESCs) as a reference point for established pluripotency. Biological replicates were collected to assay for chromatin accessibility (paired-end ATAC-seq), gene activity (single-end RNA-seq), H3K27ac ChIP-seq (single-end) in MEFs, day3, 6, 9 and PSCs. KLF4 binding (single-end ChIP-seq) was assessed in day3, 6, 9 and PSCs. KLF4/H3K27ac centric looping (paired-end Hi-ChIP) was studied in either day3, day6 and PSCs for KLF4 or MEFs and PSCs for H3K27ac.
Sample: EC-EA-3702-INPUT_DAY9
SAMN08963142 • SRS3205020 • All experiments • All runs
Organism: Mus musculus
Library:
Instrument: Illumina HiSeq 2500
Strategy: ChIP-Seq
Source: GENOMIC
Selection: ChIP
Layout: SINGLE
Construction protocol: Cells were crosslinked in 1% formaldehyde at RT for 10 minutes and quenched with 125mM glycine for 5 mins at RT. 50 million cells were used for KLF4 ChIPs and 10 million for H3K27acetylation ChIP. Cell pellets were washed twice in PBS and resuspended in 400ul lysis buffer (10mM Tris pH8, 1mM EDTA, 0.5% SDS) per 20 million cells. Cells were sonicated in a bioruptor device (30 cycles 30sec on/off, high setting) and spun down 10 minutes at 4°C at maximum speed. Supernatants were diluted 5 times with dilution buffer (0.01%SDS, 1.1% triton,1.2mM EDTA,16.7mM Tris pH8, 167mM NaCl) and incubated with the respective antibody (2-3ug/10M cells) (KLF4 R&D #3158, H3K27ac ab4729) O/N with rotation at 4°C. Next day, protein G Dynabeads (ThermoScientific) preblocked with BSA protein (100ng per 10ul Dynabeads) were added (10ul blocked Dynabeads per 10 million cells) and incubated for 2-3 hours at 4°C. Beads were immobilized on a magnet and washed twice in low salt buffer (0.1% SDS,1% triton, 2mM EDTA, 150mM NaCl, 20mM Tris pH8), twice in high salt buffer (0.1% SDS,1% triton, 2mM EDTA, 500mM NaCl, 20mM Tris pH8), twice in LiCl buffer (0.25M LiCl, 1% NP40, 1% deoxycholic acid (sodium salt), 1mM EDTA, 10mM Tris pH8) and once in TE. DNA was then eluted from the beads by incubating with 150ul elution buffer (1% SDS, 100mM NaHCO3) for 20 minutes at 65°C (vortexing every 10min). Supernatants were collected and reverse-crosslinked by incubation at 65°C O/N in presence of proteinase K. After RNase A treatment for 1hr at 37°C, DNA was purified using the minElute kit (Qiagen). 6-10ng of immunoprecipitated material was used for ChIP-seq library preparation using the KAPA Hyper prep kit (KAPA Biosystems). Libraries were sequenced on an Illumina HiSeq 2500 platform on SE50 mode.
Experiment attributes:
GEO Accession: GSM3106288
Links:
Runs: 1 run, 34.5M spots, 1.8G bases, 869.4Mb
Run# of Spots# of BasesSizePublished
SRR704842334,464,4281.8G869.4Mb2019-09-07

ID:
5446928

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