A switch in bidirectional histone mark leads to differential modulation of lincRNAs involved in neuronal and hematopoietic cell differentiation from their progenitors

2020 ◽  
Vol 121 (5-6) ◽  
pp. 3451-3462
Author(s):  
Md. Wahid Murad ◽  
Md. Abdullah‐Al‐Kamran Khan ◽  
Md. Sajedul Islam ◽  
Abul Bashar Mir Md. Khademul Islam
Keyword(s):  
Cell Differentiation ◽  
Histone Mark ◽  
Hematopoietic Cell ◽  
Differential Modulation

In vitro analysis of epiblast tissue potency for hematopoietic cell differentiation

Development ◽  
1996 ◽  
Vol 122 (3) ◽  
pp. 823-830 ◽  
Author(s):  
M. Kanatsu ◽  
S.I. Nishikawa
Keyword(s):  
Cell Differentiation ◽  
Culture System ◽  
Cell Sheet ◽  
Cell Lineage ◽  
Hematopoietic Cell ◽  
Morphogenetic Protein ◽  
Hematopoietic Cell Lineage ◽  
Vitro Analysis ◽  
In Vitro Analysis

In murine embryogenesis, all cells that will constitute the embryonic structures originate from the epiblast (primitive ectoderm) tissue, the epithelial cell sheet of the gastrulating embryo. The cells of this tissue are totipotent at the beginning of gastrulation, but at the end of this period are specified to particular cell lineages. Thus, it is likely that during murine gastrulation, the potency of epiblast cells that were originally totipotent becomes restricted as development progresses. However, the mechanisms of this process are unknown. We have investigated this process in vitro, focusing on the hematopoietic cell lineage. To detect the hematogenic potency of the epiblast tissue, we established an in vitro culture system in which the hematopoietic cell differentiation of the epiblast tissue was supported by a stromal cell layer. With this culture system, we investigated the process by which this potency becomes spatially and temporally restricted during gastrulation. The results showed that hematogenic potency resides in the entire epiblast of the early- to mid-gastrulating embryo, but becomes restricted to the posterior half of the epiblast at the headfold stage. Furthermore, we showed that this process is altered by exogenous bone morphogenetic protein-4 (BMP-4) or activin A, which may be mesoderm inducers in Xenopus embryogenesis.

scholarly journals The orphan nuclear receptor EAR-2 (NR2F6) inhibits hematopoietic cell differentiation and induces myeloid dysplasia in vivo

2018 ◽  
Vol 6 (1) ◽  
Author(s):  
Christine V. Ichim ◽  
Dzana D. Dervovic ◽  
Lap Shu Alan Chan ◽  
Claire J. Robertson ◽  
Alden Chesney ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Nuclear Receptor ◽  
Hematopoietic Cell ◽  
Orphan Nuclear Receptor

Autocrine β-related interferon controls c-myc suppression and growth arrest during hematopoietic cell differentiation

Cell ◽  
1986 ◽  
Vol 46 (1) ◽  
pp. 31-40 ◽  
Author(s):  
Dalia Resnitzky ◽  
Anat Yarden ◽  
Dov Zipori ◽  
Adi Kimchi
Keyword(s):  
Cell Differentiation ◽  
Growth Arrest ◽  
Hematopoietic Cell

The Leukemic Myeloid Cell Line OMA-AML-1: AnIn VitroModel of Hematopoietic Cell Differentiation

1994 ◽  
Vol 13 (1-2) ◽  
pp. 169-178 ◽  
Author(s):  
Samuel J. Pirruccello ◽  
John D. Jackson ◽  
J. Graham Sharp
Keyword(s):  
Cell Differentiation ◽  
Cell Line ◽  
Myeloid Cell ◽  
Hematopoietic Cell ◽  
Myeloid Cell Line

AK2 Regulates Hematopoietic Cell Survival, Proliferation and Differentiation Along the T-Cell and Neutrophil Lineages

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 1315-1315
Author(s):  
Emmanuelle M. Six ◽  
Chantal Lagresle-Peyrou ◽  
Corinne Demerens-de Chappedelaine ◽  
Justine Trimouillas ◽  
Frédéric Rieux-Laucat ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
T Cell ◽  
Conflicts Of Interest ◽  
Adenine Nucleotides ◽  
Severe Combined Immunodeficiency ◽  
T Cell Differentiation ◽  
Hematopoietic Cell ◽  
Hl60 Cell ◽  
Efficient Energy Transfer ◽  
Knock Down

Abstract Abstract 1315 AK2 deficiency is responsible for Reticular Dysgenesis (RD), a rare form of human Severe Combined Immunodeficiency which is characterized by the absence of blood neutrophils and T lymphocytes. AK2 which is located in the mitochondria interspace, plays an important role in energy metabolism and in efficient energy transfer through conversion of ADP into ATP and AMP and regulation of cellular adenine nucleotides homeostasis. We modelled the RD pathology using a lentiviral-mediated RNA interference strategy to knock-down AK2 expression. Human CD34+ progenitors invalidated for AK2 are deeply affected in their proliferative ability during the process of T-cell differentiation. Between 3 to 7 days after initiation of T-cell differentiation on the OP9-Delta1 stroma, we observed an increased cell apoptosis through disruption of the mitochondrial membrane potential, associated with a 2-fold decreased in the percentage of proliferative cells. In the presence of shAK2, the apparition of CD7+ T-cell precursors was profoundly reduced - as compared to the shControl - showing that the process of differentiation itself was affected. We also demonstrated that AK2 knock-down inhibits neutrophil differentiation using both G-CSF-mediated differentiation of CD34+ progenitors and ATRA-mediated differentiation of the HL60 cell line. In the HL60 system, we showed that the survival defect induced by the shAK2 could be rescued by expression of the anti-apoptotic protein Bcl-2, while this latter was not sufficient to restore a normal differentiation process. These data suggest a novel mechanism in which AK2 regulates not only the process of differentiation but also survival and proliferation of hematopoietic cell lineages. Disclosures: No relevant conflicts of interest to declare.

scholarly journals A Novel Ubiquitin-Specific Protease, UBP43, Cloned from Leukemia Fusion Protein AML1-ETO-Expressing Mice, Functions in Hematopoietic Cell Differentiation

1999 ◽  
Vol 19 (4) ◽  
pp. 3029-3038 ◽  
Author(s):  
Li-Qin Liu ◽  
Robert Ilaria ◽  
Paul D. Kingsley ◽  
Atsushi Iwama ◽  
Richard A. van Etten ◽  
...  
Keyword(s):  
Cell Differentiation ◽  
Cell Lines ◽  
Fetal Liver ◽  
Myeloid Cell ◽  
Protein Translation ◽  
Hematopoietic Cell ◽  
Representational Difference Analysis ◽  
Nucleotide Sequence Analysis ◽  
Monocytic Cell ◽  
Protein Ubiquitination

ABSTRACT Using PCR-coupled subtractive screening-representational difference analysis, we have cloned a novel gene from AML1-ETO knockin mice. This gene is highly expressed in the yolk sac and fetal liver of the knockin mice. Nucleotide sequence analysis indicates that its cDNA contains an 1,107-bp open reading frame encoding a 368-amino-acid polypeptide. Further protein sequence and protein translation analysis shows that it belongs to a family of ubiquitin-specific proteases (UBP), and its molecular mass is 43 kDa. Therefore, we have named this gene UBP43. Like other ubiquitin proteases, the UBP43 protein has deubiquitinating enzyme activity. Protein ubiquitination has been implicated in many important cellular events. In wild-type adult mice, UBP43 is highly expressed in the thymus and in peritoneal macrophages. Among nine different murine hematopoietic cell lines analyzed, UBP43 expression is detectable only in cell lines related to the monocytic lineage. Furthermore, its expression is regulated during cytokine-induced monocytic cell differentiation. We have investigated its function in the hematopoietic myeloid cell line M1. UBP43 was introduced into M1 cells by retroviral gene transfer, and several high-expressing UBP43 clones were obtained for further study. Morphologic and cell surface marker examination of UBP43/M1 cells reveals that overexpression of UBP43 blocks cytokine-induced terminal differentiation of monocytic cells. These data suggest that UBP43 plays an important role in hematopoiesis by modulating either the ubiquitin-dependent proteolytic pathway or the ubiquitination state of another regulatory factor(s) during myeloid cell differentiation.

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