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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Effect of TIF1γ gene deletion on hematopoietic stem cells

ABSTRACT: Analysis of KLS cells purified from bone marrow of mice conditionally inactivated for TIF1γ gene. TIF1γ deletion results in multiple defects in adult hematopoiesis. Results provide insight into the role of TIF1γ in hematopoietic stem cells functions. We used microarrays to characterize the molecular mechanisms underlying the biological properties of KLS cells lacking TIF1γ KLS (lin-,c-kit+, Sca+) cells were purified by cell sorting

ORGANISM(S): Mus musculus

SUBMITTER: Doulaye Dembele

PROVIDER: E-GEOD-22280 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Adult hematopoiesis is regulated by TIF1γ, a repressor of TAL1 and PU.1 transcriptional activity.

Kusy Sophie S Gault Nathalie N Ferri Federica F Lewandowski Daniel D Barroca Vilma V Jaracz-Ros Agnieszka A Losson Regine R Romeo Paul-Henri PH

Cell stem cell 20110401 4

Crosstalk between transcription factors and cytokines precisely regulates tissue homeostasis. Transcriptional intermediary factor 1γ (TIF1γ) regulates vertebrate hematopoietic development, can control transcription elongation, and is a component of the TGF-β signaling pathway. Here we show that deletion of TIF1γ in adult hematopoiesis is compatible with life and long-term maintenance of essential blood cell lineages. However, loss of TIF1γ results in deficient long-term hematopoietic stem cell ( ...[more]

PMID: 21474105

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Effect of TIF1γ gene deletion on hematopoietic stem cells

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Project description:Increased expression of Kruppel like factor 7 (KLF7) is an independent predictor of poor outcome in pediatric acute lymphoblastic leukemia. The contribution of KLF7 to hematopoiesis has not been previously described. Herein, we characterized the effect on murine hematopoiesis of the loss of KLF7 and enforced expression of KLF7. Long-term multilineage engraftment of Klf7-/- cells was comparable to control cells, and self-renewal, as assessed by serial transplantation, was not affected. Enforced expression of KLF7 results in a marked suppression of myeloid progenitor cell growth and a loss of short- and long-term repopulating activity. Interestingly, enforced expression of KLF7, while resulting in multi-lineage growth suppression that extended to hematopoietic stem cells and common lymphoid progenitors, spared T cells and enhanced the survival of early thymocytes. RNA expression profiling of KLF7-overexpressing hematopoietic progenitors identified several potential target genes mediating these effects. Notably, the known KLF7 target Cdkn1a (p21Cip1/Waf1) was not induced by KLF7, and loss of CDKN1A does not rescue the repopulating defect. These results suggest that KLF7 is not required for normal hematopoietic stem and progenitor (HSPC) function, but increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation and promotes early thymocyte survival. KLF7 KO vs WT HSPC expression array: KLS (lineage- c-Kit+ Sca-1+) cells were sorted from the bone marrow of Klf7-/- chimeras at 12 weeks post-transplant. Fetal liver cells were used to establish chimeric mice (C57Bl/6 background) containing a mixture of Klf7+/+ and Klf7-/- bone marrow cells.

2012-08-24 | E-GEOD-40323 | biostudies-arrayexpress

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HMGA2 overexpression

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