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Series GSE111499 Query DataSets for GSE111499
Status Public on Jul 07, 2019
Title A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling (ATAC-seq)
Organism Mus musculus
Experiment type Genome binding/occupancy profiling by high throughput sequencing
Summary Following injury, differentiated epithelial cells can serve as a stem cell-independent source for tissue regeneration by undergoing reprogramming into other cell types. The intrinsic molecular basis underlying plasticity of differentiated cells remains largely unaddressed. Here we show that Arid1a, a key component of the SWI/SNF chromatin remodeling complex, controls liver regeneration and gene expression associated with emergence of injury-induced progenitor-like cells (LPLCs). Hepatocyte-specific Arid1a ablation reduces LPLC gene expression in several models of periportal liver injury and impairs liver regeneration, leading to organ dysfunction. Arid1a establishes a permissive chromatin state at LPLC-enriched genes during homeostasis, suggesting it endows hepatocytes with competence to respond to injury-induced signals. Consistently, Arid1a facilitates binding of YAP, a critical regeneration signaling pathway, to LPLC-enriched genes, and Arid1a deletion prevents their YAP-associated induction following injury. Together, these findings provide a framework for studying the contributions of injury-induced LPLCs to periportal liver regeneration.
Overall design Normal hepatocytes and DDC-injured hepatocytes were isolated from Arid1a wild type and Arid1a liver specific KO mouse livers by a two-step liver collagenase perfusion and further purified by a series of low speed gravity centrifugation (3x2minx50g). DDC-injured hepatocytes were isolated from Sox9CreERT2:RFP reporter mice by gravity purification, and Sox9+ reprogrammed hepatocytes (LPLCs) were further isolated by sorting RFP+ hepatocytes based on the RFP expression via FACS. Biliary epithelia cells (BECs) were isolated from CK19CreERT2:RFP reporter mice by sorting RFP+ non parenchymal cells based on the RFP expression via FACS. The chromatin accessibility of normal hepatocytes, DDC-injured hepatocytes, LPLCs and BECs were identified via ATAC-seq.
Please note that each processed data .bw file was generated from both replicate samples and is linked to the corresponding Rep1 sample records.
Contributor(s) Li W, Hui L
Citation(s) 31271748
Submission date Mar 07, 2018
Last update date Oct 06, 2019
Contact name Lijian Hui
Organization name CEMCS, CAS
Department SIBCB
Lab Huilab
Street address yueyang road 320
City Shanghai
ZIP/Postal code 200031
Country China
Platforms (1)
GPL21273 HiSeq X Ten (Mus musculus)
Samples (11)
GSM3032382 ATAC_NoDDC_WT-Rep1
GSM3032383 ATAC_NoDDC_WT-Rep2
GSM3032384 ATAC_NoDDC_KO-Rep1
This SubSeries is part of SuperSeries:
GSE111502 A homeostatic Arid1a-dependent permissive chromatin state licenses hepatocyte responsiveness to liver injury-associated YAP signaling
BioProject PRJNA437239
SRA SRP134083

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource 257.1 Mb (ftp)(http) BW 249.6 Mb (ftp)(http) BW 255.6 Mb (ftp)(http) BW 219.6 Mb (ftp)(http) BW 227.3 Mb (ftp)(http) BW
GSE111499_RAW.tar 237.0 Mb (http)(custom) TAR (of BW)
SRA Run SelectorHelp
Raw data are available in SRA
Processed data are available on Series record

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