Expression data from WT and Elektra (Slfn2 mutant, loss of function) homozygous hematopoietic stem cells extracted from mice.
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PROVIDER: PRJNA929932 | ENA |
REPOSITORIES: ENA
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Project description:Expression data from WT and Elektra (Slfn2 mutant, loss of function) homozygous hematopoietic multipotent progenitor cells extracted from mice.
| PRJNA929934 | ENA
Project description:In this study we investigated the effect of Slfn2 loss of function in the murine hematopoietic system. We chose to evaluate gene expression differences in multipotent progenitors, as this population was found to be diminshed in elektra homozygous mice, additionally the MPP population also displayed increased cell cycling compared to wildtype and increased apoptosis. Abstract from associated publication copied in below, from Warsi et al. 2022 Schlafen2 is a regulator of quiescence in adult murine hematopoietic stem cells, published in Haematologica. DOI 10.3324/haematol.2021.279799 Even though hematopoietic stem cells (HSCs) are characterized by their ability to self-renew and differentiate, they primarily reside in quiescence. Despite the immense importance of this quiescent state, its maintenance and regulation is still incompletely understood. Schlafen2 (Slfn2) is a cytoplasmic protein known to be involved in cell proliferation, differentiation, quiescence, interferon response, and regulation of the immune system. Interestingly, Slfn2 is highly expressed in primitive hematopoietic cells. To investigate the role of Slfn2 in the regulation of HSCs we have studied HSC function in the elektra mouse model, where the elektra allele of the Slfn2 gene contains a point mutation causing loss of function of the Slfn2 protein. We found that homozygosity for the elektra allele caused a decrease of primitive hematopoietic compartments in murine bone marrow. We further found that transplantation of elektra bone marrow and purified HSCs resulted in a significantly reduced regenerative capacity of HSCs in competitive transplantation settings. Importantly, we found that a significantly higher fraction of elektra HSCs (as compared to WT HSCs) were actively cycling, suggesting that the mutation in Slfn2 increases HSC proliferation. This additionally caused an increased amount of apoptotic stem and progenitor cells. Taken together, our findings demonstrate that dysregulation of Slfn2 results in a functional deficiency of primitive hematopoietic cells, which is particularly reflected by a drastically impaired ability to reconstitute the hematopoietic system following transplantation and an increase in HSC proliferation. This study thus identifies Slfn2 as a novel and critical regulator of a dult HSCs and HSC quiescence.
2023-02-09 | GSE224122 | GEO
Project description:Abstract copied in below, from Warsi et al. 2022 Schlafen2 is a regulator of quiescence in adult murine hematopoietic stem cells, published in Haematologica. DOI 10.3324/haematol.2021.279799 Even though hematopoietic stem cells (HSCs) are characterized by their ability to self-renew and differentiate, they primarily reside in quiescence. Despite the immense importance of this quiescent state, its maintenance and regulation is still incompletely understood. Schlafen2 (Slfn2) is a cytoplasmic protein known to be involved in cell proliferation, differentiation, quiescence, interferon response, and regulation of the immune system. Interestingly, Slfn2 is highly expressed in primitive hematopoietic cells. To investigate the role of Slfn2 in the regulation of HSCs we have studied HSC function in the elektra mouse model, where the elektra allele of the Slfn2 gene contains a point mutation causing loss of function of the Slfn2 protein. We found that homozygosity for the elektra allele caused a decrease of primitive hematopoietic compartments in murine bone marrow. We further found that transplantation of elektra bone marrow and purified HSCs resulted in a significantly reduced regenerative capacity of HSCs in competitive transplantation settings. Importantly, we found that a significantly higher fraction of elektra HSCs (as compared to WT HSCs) were actively cycling, suggesting that the mutation in Slfn2 increases HSC proliferation. This additionally caused an increased amount of apoptotic stem and progenitor cells. Taken together, our findings demonstrate that dysregulation of Slfn2 results in a functional deficiency of primitive hematopoietic cells, which is particularly reflected by a drastically impaired ability to reconstitute the hematopoietic system following transplantation and an increase in HSC proliferation. This study thus identifies Slfn2 as a novel and critical regulator of a dult HSCs and HSC quiescence.
2023-02-09 | GSE224120 | GEO
Project description:Expression data from WT and BMPR2 knockout hematopoietic stem cells extracted from mice.
| PRJNA862726 | ENA
Project description:We investigated the role of mTORC1 in murine hematopoiesis by conditionally deleting the Raptor gene in murine hematopoietic stem cells. We observed mutliple alterations evoked by Raptor loss in hematopoiesis and profiled gene-expression alterations induced by raptor loss in Flt3-Lin-Sca1+cKit+ hematopoietic stem and progenitor enriched cell populations, 5 weeks post Raptor deletion. Flt3-Lin-Sca1+cKit+ cells were flow sorted from mice containing homozygous floxed alleles for exon 6 of the Raptor gene in the presence (MT group) or absence (WT group) of the MxCre transgene, which was induced with injections of mice with pIpC 5 weeks before cell isolation.
2012-09-19 | E-GEOD-32265 | biostudies-arrayexpress
Project description:To asses the effect of Apc loss on the intestinal epithelium we induced homozygous VillinCreERT2 Apc flox/flox mice with tamoxifen on 3 consecutive days (day 0, 1 and 2), and harvested small intestinal epithelium on day 3.
2017-06-15 | GSE83333 | GEO
Project description:Abstract copied in below, from Warsi et al. 2021 BMP signaling is required for postnatal murine hematopoietic stem cell self-renewal, published in Haematologica. DOI 10.3324/haematol.2019.236125 Life-long production of blood from hematopoietic stem cells (HSCs) is a process of strict modulation. Intrinsic and extrinsic signals govern fate options like self-renewal - a cardinal feature of HSCs. Bone morphogenetic proteins (BMP) have an established role in embryonic hematopoiesis, but less is known about its functions in adulthood. Previously, SMAD-mediated BMP signaling has been proven dispensable for HSCs. However, the BMP Type II receptor (BMPR-II) is highly expressed in HSCs, leaving the possibility that BMPs function via alternative pathways. Here, we establish that BMP signaling is required for self-renewal of adult HSCs. Through conditional knockout we show that BMPR-II deficient HSCs have impaired self-renewal and regenerative capacity. BMPR-II deficient cells have reduced p38 activation, implying that non-SMAD pathways operate downstream of BMPs in HSCs. Indeed, a majority of primitive hematopoietic cells do not engage in SMAD-mediated responses downstream of BMPs in vivo. Furthermore, deficiency of BMPR-II results in increased expression of TJP1, a known regulator of self-renewal in other stem cells, and knockdown of TJP1 in primitive hematopoietic cells partly rescues the BMPR-II null phenotype. This suggests TJP1 may be a universal stem cell regulator. In conclusion, BMP signaling, in part mediated through TJP1, is required endogenously by adult HSCs to maintain self-renewal capacity and proper resilience of the hematopoietic system during regeneration.
2022-07-28 | GSE209862 | GEO
Project description:Hematopoietic stem cell enriched Lin-Sca1+cKit+ cells were isolated from heterozygous and homozygous transgenic mice with a loxP-flanked Meis1 allele following in vivo allele deletion.
2016-02-04 | E-MTAB-4133 | biostudies-arrayexpress
Project description:Increasing evidence links metabolic activity and cell growth to decline in hematopoietic stem cell (HSC) function during aging. The Lin28b/Hmga2 pathway controls tissue development and in the hematopoietic system the postnatal downregulation of this pathway causes a decrease in self renewal of adult HSCs compared to fetal HSCs. Igf2bp2 is an RNA binding protein and a mediator of the Lin28b/Hmga2 pathway, which regulates metabolism and growth signaling by influencing RNA stability and translation of its target genes. It is currently unknown whether Lin28/Hmga2/Igf2bp2 signaling impacts on aging-associated impairments in HSC function and hematopoiesis. Here, we analyzed homozygous Igf2bp2 germline knockout mice and wildtype control animals to address this question. The study shows that Igf2bp2 deletion rescues aging phenotypes of the hematopoietic system, such as the expansion of HSC numbers in bone marrow and the biased increase of myeloid cells in peripheral blood. This rescue of hematopoietic aging coincides with reduced mitochondrial metabolism and glycolysis in Igf2bp2-/- HSCs compared to Igf2bp2+/+ HSCs. Conversely, Igf2bp2 overexpression activates protein synthesis pathways in HSCs and leads to a rapid loss of self renewal by enhancing myeloid skewed differentiation in an mTOR/PI3K-dependent manner. Together, these results show that Igf2bp2 regulates energy metabolism and growth signaling in HSCs and that the activity of this pathways influences self renewal, differentiation, and aging of HSCs.
2024-05-21 | PXD018535 | Pride
Project description:Expression profiling of D. melanogaster biniou homozygous mutant embryos in a timecourse of embryogenesis. Five one-hour timepoints were assayed (5-10 hrs, 13-14 hrs after egg laying). Homozygous mutant embryos were collected using GFP-activated embryo sorting at the same time as stage-matched wildtype controls. Four independent collections were performed at each timepoint. Total RNA was extracted and amplified. Mutant and respective wildtype samples were hybridized together on INDAC oligo-arrays.
2007-10-11 | E-TABM-250 | biostudies-arrayexpress