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Analysis of differentially expressed genes in murine Satb1-deficient hematopoietic stem cells (HSCs) compared to wild-type HSCs

ABSTRACT: Gene expression analysis on purified murine hematopoietic stem cells (HSCs) deficient for Special AT-rich sequence-binding protein 1 (Satb1) compared to wild-type HSCs. Analysis of gene expression of bone marrow-derived CD45.2+ CD150+cKit+Sca-1+CD4-CD8a-CD19-B220-Gr-1- HSCs from congenic recipient animals transplanted >20 weeks with either wild-type or Satb1-deficient hematopoeitic cells.

ORGANISM(S): Mus musculus

SUBMITTER: Boris Bartholdy

PROVIDER: E-GEOD-44107 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Satb1 regulates the self-renewal of hematopoietic stem cells by promoting quiescence and repressing differentiation commitment.

Will Britta B Vogler Thomas O TO Bartholdy Boris B Garrett-Bakelman Francine F Mayer Jillian J Barreyro Laura L Pandolfi Ashley A Todorova Tihomira I TI Okoye-Okafor Ujunwa C UC Stanley Robert F RF Bhagat Tushar D TD Verma Amit A Figueroa Maria E ME Melnick Ari A Roth Michael M Steidl Ulrich U

Nature immunology 20130407 5

How hematopoietic stem cells (HSCs) coordinate the regulation of opposing cellular mechanisms such as self-renewal and differentiation commitment remains unclear. Here we identified the transcription factor and chromatin remodeler Satb1 as a critical regulator of HSC fate. HSCs lacking Satb1 had defective self-renewal, were less quiescent and showed accelerated lineage commitment, which resulted in progressive depletion of functional HSCs. The enhanced commitment was caused by less symmetric sel ...[more]

PMID: 23563689

Similar Datasets

Analysis of differentially expressed genes in murine Satb1-deficient hematopoietic stem cells (HSCs) compared to wild-type HSCs

Project description:Gene expression analysis on purified murine hematopoietic stem cells (HSCs) deficient for Special AT-rich sequence-binding protein 1 (Satb1) compared to wild-type HSCs.

2013-04-07 | GSE44107 | GEO

Transcriptome analysis of SATB1- and SATB1+ Hematopoietic stem cells.

Project description:Hematopoietic stem cells (HSCs) are now recognized as a heterogeneous population in self-renewing and differentiation capabilities. However, fundamental mechanisms governing the heterogeneity remain uncertain. We here show that special AT-rich sequence-binding protein 1 (SATB1), a global chromatin organizer, is involved in the mechanisms. Analyzing hematological lineage-restricted SATB1 knock out mice proved that SATB1 is indispensable for both self-renewal and normal differentiation of adult HSCs. Using SATB1/Tomato knock-in mice, we subdivided HSCs according to SATB1 intensity. Culture experiments and RNA-sequencing revealed essential differences between SATB1- and SATB1+ HSCs regarding lineage potential.

2018-06-14 | GSE94630 | GEO

Expression data from Satb1- and control-transduced LSK Flt3- cells

Project description:How hematopoietic stem cells (HSCs) produce specific lineages is not well understood. We searched for key factors that direct HSC to lymphopoiesis. Comparing gene expression profiles for HSCs and early lymphoid progenitors revealed that Satb1, a global chromatin regulator, was significantly induced with lymphoid lineage specification. HSCs from Satb1-null mouse were defective in lymphopoietic activity in culture, and failed to reconstitute T-lymphopoiesis in wild-type recipients. Furthermore, Satb1-transduction in HSCs, as well as in embryonic stem cells, robustly promoted their differentiation toward lymphocytes in culture. We prepared RNA samples from control or Satb1-transfected Lin- c-kitHi Sca-1+ Flt3- cells derived from WT mouse bone marrow.

2013-04-01 | E-GEOD-45566 | biostudies-arrayexpress

Genes affected by Satb1 deficiency in HSC, LMPP and CLP

Project description:To understand gene expression signatures between wild-type and Satb1-deficient cells To examine genes regulated by Satb1 expression, sets of microarrays were conducted with Lin- c-kitHi Sca-1+ Flt3- HSC-enriched cells, Lin- c-kitHi Sca-1+ Flt3+LMPP-enriched cells, and Lin- c-kitLo Sca-1Lo IL7RÎ±+ CLP-enriched cells derived from E18.5 FL of Satb1-null mice or their WT littermates.

2013-03-20 | E-GEOD-45299 | biostudies-arrayexpress

Expression data from Satb1- and control-transduced LSK Flt3- cells

2013-04-01 | GSE45566 | GEO

Satb1

Project description:Satb1

| PRJNA788921 | ENA

Differentially regulated genes in control and c-myc N-myc deficient LT-HSCs

Project description:Analysis of HSCs from control and c-myc N-myc deficient long-term hematopoietic stem cells. HSCs lacking both c-myc and N-myc display increased apoptosis rates. Data provide insight into the molecular changes occuring upon complete loss of Myc activity, clarifying the resulting apoptotic mechanism and the role of Myc family proteins in HSCs. LT-HSC (Lin-Sca1+CD150+CD48-) cells were sorted from the BM of MxCre c-myc flox2 N-myc flox2 (experimental) and c-myc flox2 N-myc flox2 (control) mice 3 days after the last pI-pC injection. Each condition was analysed in triplicates, with each replicate consisting of a pool of 3 dKO mice or 2 control mice.

2009-02-20 | E-GEOD-12467 | biostudies-arrayexpress

Genes affected by Satb1 deficiency in HSC, LMPP and CLP

Project description:To understand gene expression signatures between wild-type and Satb1-deficient cells

2013-03-20 | GSE45299 | GEO

Genome-wide maps of DNA cytosine methylation state in during normal differentiation commitment in hematopoietic stem cells (HSC) and in Special AT-rich sequence-binding protein1 (Satb1) - deficient HSC

Project description:Our data show Satb1 deficiency leads to alterations in DNA cytosine methylation and a commitment-primed epigenetic state in HSCs. Examination of DNA cytosine methylation in wild type HSC and differentiation-committed progenitors as well as in wild type HSC and HSC lacking Satb1 (n=2 each).

2013-04-07 | E-GEOD-44304 | biostudies-arrayexpress

Next Generation Sequencing Facilitates Quantitative Analysis of Wild Type and Uhrf1-/- fetal liver hematopoietic stem cell (FL-HSCs) Transcriptomes

Project description:To investigate the molecular mechanism of Uhrf1 in controlling the self-renewal versus differentiation of FL-HSCs, high-throughput sequencing was performed to analyze the transcriptomes of WT and Uhrf1-deficient FL-HSCs.Consistent with the erythroid-biased differentiation of Uhrf1-deficient FL-HSCs, genes involved in erythrocyte differentiation were significantly enriched in Uhrf1-deficient FL-HSCs according to the Gene Ontology (GO) enrichment analysis. We generated gene signatures specific for stemness of HSCs (stem signature) or myeloerythroid progenitors (MEP signature) by subtracting the genes expressed in WT HPC(LK)s from those expressed in WT FL-HSCs or vice versa. Of the stem signature genes, 71.28% showed lower expression and 28.72% showed higher expression in Uhrf1-deficient FL-HSCs compared with WT FL-HSCs. Interestingly, among the MEP signature genes, genes enriched in erythroid differentiation (27.54%) were up-regulated in the absence of Uhrf1, whereas the remaining genes enriched in myeloid-specific genes (72.46%) were suppressed consistent with previous research. Particularly, in comparison to the WT control, Uhrf1-deficient FL-HSCs up-regulated certain erythrocyte differentiation-related genes (e.g., Gata1, Gata2, Gfi1b, Car1, Zfpm1 and Itga2b), most of which were physiologically up-regulated in HPC(LK)s, whereas some genes (Id2, Satb1, Hmga2) that play critical roles in HSC maintenance were down-regulated. These results suggested that Uhrf1 controls the self-renewal versus differentiation of FL-HSCs by suppressing the expression of the erythroid-specific genes and maintaining the expression of HSC stemness genes.

2016-11-30 | GSE85450 | GEO

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