A transitional stage in the commitment of mesoderm to hematopoiesis requiring the transcription factor SCL/tal-1

Development ◽  
2000 ◽  
Vol 127 (11) ◽  
pp. 2447-2459 ◽  
Author(s):  
S.M. Robertson ◽  
M. Kennedy ◽  
J.M. Shannon ◽  
G. Keller
Keyword(s):  
Transcription Factor ◽  
Embryoid Body ◽  
Early Stage ◽  
Es Cells ◽  
Blast Cell ◽  
Stage Of Development ◽  
Erythroid Precursors ◽  
Identification And Characterization ◽  
Definitive Hematopoiesis

In this report, we describe the identification and characterization of an early embryoid body-derived colony, termed the transitional colony, which contains cell populations undergoing the commitment of mesoderm to the hematopoietic and endothelial lineages. Analysis of individual transitional colonies indicated that they express Brachyury as well as flk-1, SCL/tal-1, GATA-1, (beta)H1 and (beta)major reflecting the combination of mesodermal, hematopoietic and endothelial populations. This pattern differs from that found in the previously described hemangioblast-derived blast cell colonies in that they typically lacked Brachyury expression, consistent with their post-mesodermal stage of development (Kennedy, M., Firpo, M., Choi, K., Wall, C., Robertson, S., Kabrun, N. and Keller, G. (1997) Nature 386, 488–493). Replating studies demonstrated that transitional colonies contain low numbers of primitive erythroid precursors as well as a subset of precursors associated with early stage definitive hematopoiesis. Blast cell colonies contain higher numbers and a broader spectrum of definitive precursors than found in the transitional colonies. ES cells homozygous null for the SCL/tal-1 gene, a transcription factor known to be essential for development of the primitive and definitive hematopoietic systems, were not able to form blast colonies but did form transitional colonies. Together these findings suggest that the transitional colony represents a stage of development earlier than the blast cell colony and one that uniquely defines the requirement for a functional SCL/tal-1 gene for the progression to hematopoietic commitment.

scholarly journals Erythroid-cell-specific properties of transcription factor GATA-1 revealed by phenotypic rescue of a gene-targeted cell line.

1997 ◽  
Vol 17 (3) ◽  
pp. 1642-1651 ◽  
Author(s):  
M J Weiss ◽  
C Yu ◽  
S H Orkin
Keyword(s):  
Transcription Factor ◽  
Cell Line ◽  
Zinc Finger ◽  
Es Cells ◽  
Embryonic Stem ◽  
Erythroid Cell ◽  
Transactivation Domain ◽  
Stage Of Development ◽  
Erythroid Maturation

The zinc finger transcription factor GATA-1 is essential for erythropoiesis. In its absence, committed erythroid precursors arrest at the proerythroblast stage of development and undergo apoptosis. To study the function of GATA-1 in an erythroid cell environment, we generated an erythroid cell line from in vitro-differentiated GATA-1- murine embryonic stem (ES) cells. These cells, termed G1E for GATA-1- erythroid, proliferate as immature erythroblasts yet complete differentiation upon restoration of GATA-1 function. We used rescue of terminal erythroid maturation in G1E cells as a stringent cellular assay system in which to evaluate the functional relevance of domains of GATA-1 previously characterized in nonhematopoietic cells. At least two major differences were established between domains required in G1E cells and those required in nonhematopoietic cells. First, an obligatory transactivation domain defined in conventional nonhematopoietic cell transfection assays is dispensable for terminal erythroid maturation. Second, the amino (N) zinc finger, which is nonessential for binding to the vast majority of GATA DNA motifs, is strictly required for GATA-1-mediated erythroid differentiation. Our data lead us to propose a model in which a nuclear cofactor(s) interacting with the N-finger facilitates transcriptional action by GATA-1 in erythroid cells. More generally, our experimental approach highlights critical differences in the action of cell-specific transcription proteins in different cellular environments and the power of cell lines derived from genetically modified ES cells to elucidate gene function.

scholarly journals Characterization of intracellular free Ca2+ movements in neural progenitor cells derived from ES cells transfected with MASH1 transcription factor gene

Ensho Saisei ◽  
2005 ◽  
Vol 25 (5) ◽  
pp. 452-460 ◽  
Author(s):  
Michiko Ide ◽  
Yuji Ueda ◽  
Kenji Watanabe ◽  
Manae S. Kurokawa ◽  
Hideshi Yoshikawa ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Progenitor Cells ◽  
Neural Progenitor Cells ◽  
Es Cells ◽  
Neural Progenitor ◽  
Transcription Factor Gene ◽  
Factor Gene

scholarly journals Identification and characterization of constrained non-exonic bases lacking predictive epigenomic and transcription factor binding annotations

2019 ◽  
Author(s):  
Olivera Grujic ◽  
Tanya N. Phung ◽  
Soo Bin Kwon ◽  
Adriana Arneson ◽  
Yuju Lee ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Transcription Factor Binding ◽  
Regulatory Sequence ◽  
Human Genetic Variation ◽  
Sequence Motifs ◽  
Variant Prioritization ◽  
Factor Binding ◽  
Genome Wide ◽  
Identification And Characterization

AbstractAnnotations of evolutionarily constraint provide important information for variant prioritization. Genome-wide maps of epigenomic marks and transcription factor binding provide complementary information for interpreting a subset of such prioritized variants. Here we developed the Constrained Non-Exonic Predictor (CNEP) to quantify the evidence of each base in the human genome being in a constrained non-exonic element from over 60,000 epigenomic and transcription factor binding features. We find that the CNEP score outperforms baseline and related existing scores at predicting constrained non-exonic bases from such data. However, a subset of such bases are still not well predicted by CNEP. We developed a complementary Conservation Signature Score by CNEP (CSS-CNEP) using conservation state and constrained element annotations that is predictive of those bases. Using human genetic variation, regulatory sequence motifs, mouse epigenomic data, and retrospectively considered additional human data we further characterize the nature of constrained non-exonic bases with low CNEP scores.

scholarly journals Identification and Characterization of aSchizosaccharomyces pombeRNA Polymerase II Elongation Factor with Similarity to the Metazoan Transcription Factor ELL

2006 ◽  
Vol 282 (8) ◽  
pp. 5761-5769 ◽  
Author(s):  
Charles A. S. Banks ◽  
Stephanie E. Kong ◽  
Henrik Spahr ◽  
Laurence Florens ◽  
Skylar Martin-Brown ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Elongation Factor ◽  
Identification And Characterization

scholarly journals Identification and Characterization of Aspergillus nidulans Mutants Impaired in Asexual Development under Phosphate Stress

Cells ◽  
2019 ◽  
Vol 8 (12) ◽  
pp. 1520 ◽  
Author(s):  
Ainara Otamendi ◽  
Eduardo A. Espeso ◽  
Oier Etxebeste
Keyword(s):  
Transcription Factor ◽  
Aspergillus Nidulans ◽  
Genomic Library ◽  
Phenotypic Trait ◽  
Mutant Form ◽  
Multicopy Suppressor ◽  
Putative Transcription Factor ◽  
Recessive Mutant ◽  
Identification And Characterization

The transcription factor BrlA plays a central role in the production of asexual spores (conidia) in the fungus Aspergillus nidulans. BrlA levels are controlled by signal transducers known collectively as UDAs. Furthermore, it governs the expression of CDP regulators, which control most of the morphological transitions leading to the production of conidia. In response to the emergence of fungal cells in the air, the main stimulus triggering conidiation, UDA mutants such as the flbB deletant fail to induce brlA expression. Nevertheless, ΔflbB colonies conidiate profusely when they are cultured on a medium containing high H2PO4− concentrations, suggesting that the need for FlbB activity is bypassed. We used this phenotypic trait and an UV-mutagenesis procedure to isolate ΔflbB mutants unable to conidiate under these stress conditions. Transformation of mutant FLIP166 with a wild-type genomic library led to the identification of the putative transcription factor SocA as a multicopy suppressor of the FLIP (Fluffy, aconidial, In Phosphate) phenotype. Deregulation of socA altered both growth and developmental patterns. Sequencing of the FLIP166 genome enabled the identification and characterization of PmtCP282L as the recessive mutant form responsible for the FLIP phenotype. Overall, results validate this strategy for identifying genes/mutations related to the control of conidiation.

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