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Gene expression data of Lsd1fl/fl and Lsd1fl/fl EpoRCre CD71_high / c-Kit_high pro-erythroblasts.

ABSTRACT: We discovered that mice lacking Lsd1 in the erythroid lineage die in utero of a lethal anemia around embryonic day E13.5. Lsd1 knockout embryos displayed an increase in CD71_high c-Kit_high pro-erythroblasts, followed by a drastic reduction of later maturation stages. To determine the genes altered by Lsd1-loss, CD71_high c-Kit_high pro-erythroblasts from Lsd1fl/fl and Lsd1fl/fl EpoRCre mice were FACS-purified to be analyzed by gene expression profiling.

ORGANISM(S): Mus musculus

PROVIDER: GSE40283 | GEO | 2013/06/25

SECONDARY ACCESSION(S): PRJNA173407

REPOSITORIES: GEO

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Gene expression data of Lsd1fl/fl and Lsd1fl/fl EpoRCre CD71_high / c-Kit_high pro-erythroblasts.

Project description:We discovered that mice lacking Lsd1 in the erythroid lineage die in utero of a lethal anemia around embryonic day E13.5. Lsd1 knockout embryos displayed an increase in CD71_high c-Kit_high pro-erythroblasts, followed by a drastic reduction of later maturation stages. To determine the genes altered by Lsd1-loss, CD71_high c-Kit_high pro-erythroblasts from Lsd1fl/fl and Lsd1fl/fl EpoRCre mice were FACS-purified to be analyzed by gene expression profiling. Primary CD71high c-Kithigh pro-erythroblasts were isolated by FACS-sorting from fetal livers of E13.5 Lsd1fl/fl and Lsd1fl/fl EpoRCre embryos. Total RNA from two biological replicates per genotype was extracted and used to hybridize to Affymetrix expression arrays using the Mouse Genome 430A array platform.

2013-06-25 | E-GEOD-40283 | biostudies-arrayexpress

Ribosomal deficiencies in Diamond-Blackfan anemia impair translation of transcripts essential for differentiation of murine and human erythroblasts

Project description:Diamond Blackfan Anemia (DBA) is associated with developmental defects and profound anemia. Mutations in genes encoding a ribosomal protein of the small (e.g. Rps19) or large (e.g. Rpl11) ribosomal subunit are found in over half of these patients. The mutations cause ribosomal haploinsufficiency, which reduces overall translation efficiency of cellular mRNAs. We reduced expression of *Rps19* or *Rpl11* in mouse erythroblasts and investigated mRNA polyribosome association, which revealed deregulated translation initiation of specific transcripts. Among these were *Bag1*, encoding a Hsp70 co-chaperone, and *Csde1*, encoding an RNA binding protein, both expressed at increased levels in erythroblasts. Their translation initiation is cap-independent and starts from an internal ribosomal entry site (IRES), which appeared sensitive to knock down of Rps19 or Rpl11. Mouse embryos lacking Bag1 die at embryonic day E13.5 with reduced erythroid colony forming cells in the fetal liver, and low Bag1 expression impairs erythroid differentiation in vitro. Reduced expression of Csde1 impairs proliferation and differentiation of erythroid blasts. Protein but not mRNA expression of *BAG1* and *CSDE1* was reduced in erythroblasts cultured from DBA patients. Our data suggest that impaired IRES-mediated translation of mRNAs expressed at increased levels in erythroblasts contributes to the erythroid phenotype of DBA. 3 biological replicates of erythroblasts treated with different shRNA were used for polyribosomal sucrose gradients; RNA was extracted from gradients in 2 samples - mRNA associated with polyribosomes (poly) and the rest (sub).

2011-11-14 | E-GEOD-22903 | biostudies-arrayexpress

MicroRNA profiling by array in of mouse bone marrow erythroblasts from Argonaute 2 deficient mice (ago2 fl/fl & ago2 -/-)

Project description:microRNA profiling in Argonaute 2 deficient mice bone marrow erythroblasts (ago2 fl/fl & ago2 -/-)

2010-05-26 | E-TABM-996 | biostudies-arrayexpress

Ribosomal deficiencies in Diamond-Blackfan anemia impair translation of transcripts essential for differentiation of murine and human erythroblasts

2011-11-14 | GSE22903 | GEO

Erythroblasts

Project description:Erythroblasts

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Gene expression data of Lsd1fl/fl and Lsd1fl/fl Mx1Cre Gr1dim Mac1 granulocytic progenitor cells.

Project description:We discovered that mice with hematopoietic-specific deletion of Lsd1 lacked Gr-1+ Mac1+ neutrophilic granulocytes whereas the numbers of Gr-1dim Mac1+ granulocytic progenitor cells was increased. To determine the genes altered by Lsd1-loss, Gr-1dim Mac1+ granulocytic progenitor cells from Lsd1fl/fl and Lsd1fl/fl Mx1Cre mice were FACS-purified to be analyzed by gene expression profiling. Primary Gr-1dim Mac1+ granulocytic progenitor cells were isolated from the bone marrow of Lsd1fl/fl and Lsd1fl/fl Mx1Cre animals by FACS-sorting, one week after the final p(I:C) dose. Total RNA from three biological replicates per genotype was extracted and used to hybridize to Affymetrix expression arrays using the Mouse Genome 430 2.0 array platform.

2013-06-25 | E-GEOD-40282 | biostudies-arrayexpress

Next generation sequencing following CUX1 knockdown in erythroblasts

Project description:Anemia is a significant cause of morbidity and mortality in myeloid malignances. Cytogenetic changes are recurrent within malignant hematopoietic stem and progenitor cells, yet their role in anemia pathogenesis remains unknown. One recurrent karyotypic abnormality in myeloid neoplasms is the deletion of part or all of chromosome 7 [-7/del(7q)], which harbors the transcription factor and tumor suppressor gene, CUX1. CUX1 knockdown mouse models develop myeloid disease similar to that seen in humans, including a spontaneous, cell intrinsic, and lethal anemia that develops with age. Here, we elucidate the cellular and molecular mechanisms by which CUX1 regulates erythropoiesis. We demonstrate CUX1 knockdown mice have an aberrant stress erythropoiesis response and decreased survival after acute anemia induction. CUX1 insufficient erythroblasts undergo accelerated cell cycling and increased apoptosis. In line with these phenotypes, transcriptome profiling indicates that CUX1-knockdown elicits increased proliferation and decreased erythroid differentiation gene signatures. ATAC-sequencing demonstrated dramatic, global chromatin opening in CUX1-knockdown erythroblasts. As measured by fluorescence lifetime imaging, this increased chromatin accessibility is concomitant with a disruption in nuclear condensation, which is normally requisite in mammalian erythroblasts for nuclear eviction and terminal differentiation. Finally, we show that CUX1 mediates chromatin compaction by promoting histone deacetylation. Thus, rather than a transcriptional role, our data implicate in an epigenetic regulatory role for CUX1 in erythropoiesis. Furthermore, these results suggest therapeutic targeting of epigenetic regulators, such as histone acetyl transferases, may have clinical benefit for the anemias associated with loss of CUX1.

2021-08-10 | GSE181626 | GEO

Gene expression data of Lsd1fl/fl and Lsd1fl/fl Mx1Cre Gr1dim Mac1 granulocytic progenitor cells.

2013-06-25 | GSE40282 | GEO

Gene expression data of Lsd1fl/fl and Lsd1fl/fl Mx1Cre CD150+ CD48- lin- c-Kit+ Sca-1+ LT-HSCs

Project description:We discovered that mice that lack Lsd1 in hematopoietic cells were exhibited increased frequencies of CD150+ CD48- lin- c-Kit+ Sca-1+ LT-HSCs, but completely lacked the lin- c-Kit+ Sca-1- myeloid progenitor compartment. To determine the genes altered by Lsd1-loss, CD150+ CD48- lin- c-Kit+ Sca-1+ LT-HSCs from Lsd1fl/fl and Lsd1fl/fl Mx1Cre mice were FACS-purified to be analyzed by gene expression profiling.

2013-06-25 | GSE40284 | GEO

Iron deficiency anemia in mice involves alterations in mitophagy and gene expression in erythroblasts

Project description:Since iron deficiency anemia (IDA) is one of the most common diseases in worldwide, it is an essential issue to prevent and to treat the IDA in public healthcare system. However, the precise adaptive responses and their mechanisms of the hematopoietic system induced by iron deficient state are not fully understood. In this study, low iron diet conditions which induce sever iron deficiency anemia in mice were established. Transcriptome analyses in erythroblasts under normal or iron deficient states were performed to describe the pathological details of IDA. Under iron deficient state, extensive gene expression changes and mitophagy disorder were induced during the terminal maturation of erythroblasts. These findings provide a new insight into pathophysiology and molecular biology of IDA and the function of iron as a coordinator of gene expression networks in erythrocyte maturation.

2016-12-14 | GSE77694 | GEO

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