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UG4 enhancer-driven GATA-2 and bone morphogenetic protein 4 complementation remedies the CAKUT phenotype in Gata2 hypomorphic mutant mice.
Ainoya K, Moriguchi T, Ohmori S, Souma T, Takai J, Morita M, Chandler KJ, Mortlock DP, Shimizu R, Engel JD, Lim KC, Yamamoto M
(2012) Mol Cell Biol 32: 2312-22
MeSH Terms: Animals, Bone Morphogenetic Protein 4, Enhancer Elements, Genetic, GATA2 Transcription Factor, Gene Expression Regulation, Developmental, Mesoderm, Mice, Mutation, Urogenital Abnormalities, Urogenital System, Vesico-Ureteral Reflux
Show Abstract · Added May 27, 2014
During renal development, the proper emergence of the ureteric bud (UB) from the Wolffian duct is essential for formation of the urinary system. Previously, we showed that expression of transcription factor GATA-2 in the urogenital primordium was demarcated anteroposteriorly into two domains that were regulated by separate enhancers. While GATA-2 expression in the caudal urogenital mesenchyme is controlled by the UG4 enhancer, its more-rostral expression is regulated by UG2. We found that anteriorly displaced budding led to obstructed megaureters in Gata2 hypomorphic mutant mice, possibly due to reduced expression of the downstream effector bone morphogenetic protein 4 (BMP4). Here, we report that UG4-driven, but not UG2-driven, GATA-2 expression in the urogenital mesenchyme significantly reverts the uropathy observed in the Gata2 hypomorphic mutant mice. Furthermore, the data show that transgenic rescue by GATA-2 reverses the rostral outgrowth of the UB. We also provide evidence for a GATA-2-BMP4 epistatic relationship by demonstrating that reporter gene expression from a Bmp4 bacterial artificial chromosome (BAC) transgene is altered in Gata2 hypomorphs; furthermore, UG4-directed BMP4 expression in the mutants leads to reduced incidence of megaureters. These results demonstrate that GATA-2 expression in the caudal urogenital mesenchyme as directed by the UG4 enhancer is crucial for proper development of the urinary tract and that its regulation of BMP4 expression is a critical aspect of this function.
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11 MeSH Terms
The TAL1/SCL transcription factor regulates cell cycle progression and proliferation in differentiating murine bone marrow monocyte precursors.
Dey S, Curtis DJ, Jane SM, Brandt SJ
(2010) Mol Cell Biol 30: 2181-92
MeSH Terms: Animals, Basic Helix-Loop-Helix Transcription Factors, Cell Cycle, Cell Differentiation, Cell Line, Cell Proliferation, Cell Survival, Cyclin-Dependent Kinase Inhibitor p16, DNA, GATA2 Transcription Factor, Gene Expression Regulation, Gene Knockout Techniques, Introns, Leukopoiesis, Mice, Mice, Knockout, Monocytes, Protein Binding, Proto-Oncogene Proteins, RNA, Messenger, Stem Cells, T-Cell Acute Lymphocytic Leukemia Protein 1, beta-Galactosidase
Show Abstract · Added March 5, 2014
Monocytopoiesis involves the stepwise differentiation in the bone marrow (BM) of common myeloid precursors (CMPs) to monocytes. The basic helix-loop-helix transcription factor TAL1/SCL plays a critical role in other hematopoietic lineages, and while it had been reported to be expressed by BM-derived macrophages, its role in monocytopoiesis had not been elucidated. Using cell explant models of monocyte/macrophage (MM) differentiation, one originating with CMPs and the other from more committed precursors, we characterized the phenotypic and molecular consequences of inactivation of Tal1 expression ex vivo. While Tal1 knockout had minimal effects on cell survival and slightly accelerated terminal differentiation, it profoundly inhibited cell proliferation and decreased entry into and traversal of the G(1) and S phases. In conjunction, steady-state levels of p16(Ink4a) mRNA were increased and those of Gata2 mRNA decreased. Chromatin immunoprecipitation analysis demonstrated the association of Tal1 and E47, one of its E protein DNA-binding partners, with an E box-GATA sequence element in intron 4 of the Gata2 gene and with three E boxes upstream of p16(Ink4a). Finally, wild-type Tal1, but not a DNA binding-defective mutant, rescued the proliferative defect in Tal1-null MM precursors. These results document the importance of this transcription factor in cell cycle progression and proliferation during monocytopoiesis and the requirement for direct DNA binding in these processes.
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23 MeSH Terms
Transcriptional link between blood and bone: the stem cell leukemia gene and its +19 stem cell enhancer are active in bone cells.
Pimanda JE, Silberstein L, Dominici M, Dekel B, Bowen M, Oldham S, Kallianpur A, Brandt SJ, Tannahill D, Gƶttgens B, Green AR
(2006) Mol Cell Biol 26: 2615-25
MeSH Terms: Animals, Basic Helix-Loop-Helix Transcription Factors, Blood, Bone and Bones, Cell Differentiation, Cells, Cultured, DNA-Binding Proteins, Enhancer Elements, Genetic, GATA2 Transcription Factor, Gene Expression Regulation, Developmental, Genes, Reporter, Mice, Mice, Transgenic, Muscle, Smooth, Vascular, Nuclear Proteins, Osteogenesis, Proto-Oncogene Protein c-fli-1, Proto-Oncogene Proteins, Skeleton, Stem Cells, T-Cell Acute Lymphocytic Leukemia Protein 1, Transcription Factors, Transcription, Genetic
Show Abstract · Added March 5, 2014
Blood and vascular cells are generated during early embryogenesis from a common precursor, the hemangioblast. The stem cell leukemia gene (SCL/tal 1) encodes a basic helix-loop-helix transcription factor that is essential for the normal development of blood progenitors and blood vessels. We have previously characterized a panel of SCL enhancers including the +19 element, which directs expression to hematopoietic stem cells and endothelium. Here we demonstrate that SCL is expressed in bone primordia during embryonic development and in adult osteoblasts. Despite consistent expression in cells of the osteogenic lineage, SCL protein is not required for bone specification of embryonic stem cells. In transgenic mice, the SCL +19 core enhancer directed reporter gene expression to vascular smooth muscle and bone in addition to blood and endothelium. A 644-bp fragment containing the SCL +19 core enhancer was active in both blood and bone cell lines and was bound in vivo by a common array of Ets and GATA transcription factors. Taken together with the recent observation that a common progenitor can give rise to blood and bone cells, our results suggest that the SCL +19 enhancer targets a mesodermal progenitor capable of generating hematopoietic, vascular, and osteoblastic progeny.
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23 MeSH Terms
Characterization of the human platelet/endothelial cell adhesion molecule-1 promoter: identification of a GATA-2 binding element required for optimal transcriptional activity.
Gumina RJ, Kirschbaum NE, Piotrowski K, Newman PJ
(1997) Blood 89: 1260-9
MeSH Terms: Base Sequence, Binding Sites, Cell Line, Transformed, DNA, DNA, Complementary, DNA-Binding Proteins, Erythroid-Specific DNA-Binding Factors, GATA1 Transcription Factor, GATA2 Transcription Factor, Gene Expression Regulation, Humans, Leukocytes, Molecular Sequence Data, Organ Specificity, Platelet Endothelial Cell Adhesion Molecule-1, Promoter Regions, Genetic, Transcription Factor AP-2, Transcription Factors, Transcription, Genetic, Transfection, Tumor Cells, Cultured
Show Abstract · Added February 21, 2015
Platelet/endothelial cell adhesion molecule-1 (PECAM-1) is a 130-kD member of the Ig gene superfamily that is expressed on platelets, endothelial cells, and certain leukocyte subsets. To examine the factors controlling vascular-specific expression of PECAM-1, we cloned the 5'-flanking region of the PECAM-1 gene and analyzed its transcriptional activity. 5'-Rapid amplification of cDNA ends (5'-RACE) analysis showed that transcription initiation occurred at several closely spaced nearby sites originating approximately 204 bp upstream from the translation start site. Analysis of the sequence immediately upstream from the transcription initiation site (TIS) showed no canonical TATA or CAAT elements, however an initiator element commonly found in TATA-less promoters encompassed the TIS. 5'-serially truncated PECAM-1 promoter segments cloned in front of a luciferase reporter drove transcription in both a lineage- and orientation-specific manner. Putative cis-acting control elements present within a 300-bp core promoter included two ets sites, an Sp1 site, tandem E-box domains, two GATA-associated sites (CACCC), an AP-2 binding site, and a GATA element at -24. Mutational analysis showed that optimal transcriptional activity required the GATA sequence at position -24, and gel-shift assays further showed that the GATA-2 transcription factor, but not GATA-1, bound to this region of the PECAM-1 promoter. Understanding the cis- and transacting factors that regulate the tissue-specific expression of PECAM-1 should increase our understanding of the mechanisms by which vascular-specific gene expression is achieved.
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21 MeSH Terms