Posterior embryonic axis develops from neuromesodermal progenitors which differentiate into neural tube and paraxial mesoderm
Recapitulating early development of mouse musculoskeletal precursors of the paraxial mesoderm <i>in vitro</i>.
Treatment
View SamplesErg is an ETS family transcription factor frequently overexpressed in human leukemias and has been implicated as a key regulator of hematopoietic stem cells (HSCs). However how Erg controls normal hematopoiesis, particularly at the stem cell level, remains poorly understood. Using homologous recombination, we generated an Erg knockdown allele (Ergkd) in which Erg expression can be restored upon Cre-mediated excision of a Stopper cassette. In Ergkd/+ mice, ~40% reduction in Erg dosage perturbed both fetal liver and bone marrow hematopoiesis by reducing the numbers of Lin-Sca-1+c-Kit+ (LSK) hematopoietic stem and progenitor cells (HSPCs) and megakaryocytic progenitors.
Reduced Erg Dosage Impairs Survival of Hematopoietic Stem and Progenitor Cells.
Specimen part
View SamplesTo understand the molecular mechanisms mediating Liver Resident Leukocytes (LRL) relocalization from the liver to the lungs in response to tumor progression, isolated LRLs from the liver and lungs of tumor-stimulating mice using a cell sorter. LRLs remaining in the liver displayed increased liver signature when compared to those that migrated into the lungs.
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Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Histone demethylase Lsd1 represses hematopoietic stem and progenitor cell signatures during blood cell maturation.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Differential roles of Sall4 isoforms in embryonic stem cell pluripotency.
Specimen part, Cell line
View SamplesMurine embryonic stem cells (ESCs) are defined by continuous self-renewal and pluripotency. A diverse repertoire of protein isoforms arising from alternative splicing are expressed in ES cells without defined biological roles. Sall4, a transcription factor essential for pluripotency, exists as two isoforms (Sall4a and Sall4b). By genome-wide location analysis, we have determined that Sall4b, and not Sall4a, binds preferentially to highly expressed loci in ES cells. Sall4a and Sall4b binding sites are distinguished by both epigenetic marks at target loci and their clustering with binding sites of other pluripotency factors. When ESCs expressing a single isoform of Sall4 are generated, Sall4b alone could maintain the pluripotent state, although it could not completely suppress all differentiation markers. Sall4a and Sall4b collaborate in maintenance of the pluripotent state, but play distinct roles. Our work is novel in establishing such isoform-specific differences in ES cells.
Differential roles of Sall4 isoforms in embryonic stem cell pluripotency.
Specimen part, Cell line
View SamplesTo determine hypoxia mediated changes in whole blood, normal C57Bl/10 mice were gradually exposed to a chronic hypoxic environment, equivalent to an altitude of 6500m, for 2 weeks in vivo. Control, age-matched mice were maintained under normoxic, normobaric conditions by exposing them to ambient air in Philadelphia (c. 50 mts above sea level).
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View SamplesTo understand hypoxia mediated changes in whole blood, normal C57Bl/10 mice were gradually exposed to a chronic chemical hypoxic environment, for 2 weeks. Control, age-machted mice were maintained under normoxic conditions.
No associated publication
No sample metadata fields
View SamplesTo determine hypoxia mediated changes in whole blood, normal swiss webster mice were gradually exposed to a chronic hypobaric hypoxic environment up to 8500m, for 2 weeks in vivo. Control, age-matched mice were maintained under normoxic conditions in Kathmandu (c. 1300 mts above sea level).
No associated publication
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View SamplesWe 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.
No associated publication
Sex, Specimen part
View Samples