Bone marrow endosteum houses Hedgehog-susceptible Dlx5-expressing osteoblast precursor cells
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ABSTRACT:
PROVIDER: PRJNA1177850 | ENA |
REPOSITORIES: ENA
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Project description:Bone marrow endosteum houses Hedgehog-susceptible Dlx5-expressing osteoblast precursor cells [Fgfr3CE_Cxcl12GFP]
| PRJNA1179926 | ENA
Project description:A single cell transcriptional profile of osteoblasts and bone marrow stromal cells of the murine femur at postnatal day 49 (P49), lineage-marked by Dlx5-creER at P21
2024-10-31 | GSE280325 | GEO
Project description:A single cell transcriptional profile of osteoblasts and bone marrow stromal cells of the murine femur at postnatal day 49 (P49), lineage-marked by Fgfr3-creER at P21
2024-11-06 | GSE280669 | GEO
Project description:Lck-Dlx5 induces T-cell lymphoma but the mechanism is unknown. We used microarrays to detail the global programme of gene expression underlying Dlx5-induced T-cell lymphoma T-cells were isolated from Lck-Dlx5 mice, Lck-MyrAkt2 mice and Wild type littermates for RNA extraction and hybridization on Affymetrix microarrays.
2016-06-24 | E-GEOD-83685 | biostudies-arrayexpress
Project description:Lck-Dlx5 induces T-cell lymphoma but the mechanism is unknown. We used microarrays to detail the global programme of gene expression underlying Dlx5-induced T-cell lymphoma
2016-06-24 | GSE83685 | GEO
Project description:Several transcription factors are known to be expressed in discrete regions of the otic vesicle and Dlx5 is one of those that is expressed highly in the presumptive dorsal vestibular region. Mice lacking Dlx5 have vestibular defects. Specifically, they fail to form the endolymphatic duct (a defect visible as early as E10) as well as the anterior and posterior semi-circular canals. The lateral canal does form but is smaller, whereas the saccule, the utricle and the cochlea appear relatively normal. The goal of this study was to use microarrays to identify differentially expressed genes between wild-type and Dlx5-null otic vesicles microdissected from E10 and 10.5 and identify downstream targets of Dlx5 by searching the immediate 3kb promoter regions of the differentially expressed genes for homeodomain binding sites followed by chromatin immunoprecipitation in an otic vesicle-derived cell line over-expressing Dlx5. Normal vestibular morphogenesis is compromised in mice lacking Dlx5, a member of the Distal-less family of homeobox transcription factors. We identified its direct downstream targets in the developing mouse inner ear by gene expression profiling wild-type and Dlx5 null otic vesicles from embryonic stages E10 and E10.5. Four hundred genes were differentially expressed in mutants when compared to wild-type in at least one of the two stages. To further constrain the list of likely direct targets of Dlx5, we examined the genomic DNA sequences in the 3kb promoter regions immediately proximal to the transcriptional start sites of these genes. We searched for (i) one or more previously described binding site for Dlx5, (ii) one or more novel 12bp-long motifs with a canonical homeodomain response element (HDRE) shared by promoters of two or more genes, and (iii) 100% conservation of the 12bp-long HDRE-containing motifs in promoter regions of human orthologs. Forty genes passed one or more of these filters, 12 of which are known to be expressed in the developing otic vesicle in domains that at least partially overlap with that of Dlx5 in one or both stages that we examined. Chromatin immunoprecipitation using a Dlx5 antibody confirmed direct binding of Dlx5 to promoter regions of seven of these genes (Atbf1, Bmper, Large, Lrrtm1, and Msx1, all of which were down-regulated in mutants, and Ebf1 and Lhx1, both of which were up-regulated in mutants) in an otic vesicle-derived cell line over-expressing Dlx5. Gene expression profiling of this cell line showed that Bmper and Lrrtm1 transcripts were up-regulated, further supporting their identification as direct targets of Dlx5 activity. Otic vesicles from wild-type and Dlx5-null embryos were microdissected from mouse developmental stages E10 and E10.5 and expression profiled in duplicate for each stage and genotype. Dlx5-transfected and empty vector-transfected 2B1 cell line samples were also profiled in duplicate (independent cell cultures).
2011-07-01 | E-GEOD-22381 | biostudies-arrayexpress
Project description:Sp7/Osterix is a master regulator of osteoblast specification. To identify the Sp7-mediated gene regulatory network in osteoblasts, we performed Sp7 ChIP-seq on primary mouse calvarial osteoblasts comparing the DNA binding profile with the transcriptional profile of Sp7-positive osteoblasts. Analysis of these identified a network of Sp7 regulated osteoblast targets and provides a new insight into the mode of Sp7 action in osteoblast. To further study for the Sp7 mode, we performed ChIP-seq for Sp1, Sp7, Dlx5, as a potential Sp7 partner identified in this study and mutated Sp7 which has mutations in the zinc finger domain, by using in vitro system with a pre-osteoblast mouse cell line, MC3T3E1.
2016-04-28 | GSE76185 | GEO
Project description:Homeobox gene Dlx5 induces T-cell lymphoma in transgenic mice. To find the target oncogene implicated in this lymphoma genesis, we immunoprecipitated Dlx5 and sequenced the bound DNA fragments.
2017-06-10 | GSE83778 | GEO
Project description:Fetal bone development occurs by endochondral conversion of avascular cartilage to vascularized bone at the growth plate. This requires coordinated mobilization of osteoblast precursors with blood vessels. In adult bone, vessel-adjacent osteoblast precursors are maintained by mechanical stimuli; however, the mechanisms by which these cells mobilize and respond to mechanical cues during embryonic development are unknown. Here, we unify osteoblast precursor co-mobilization and mechanotransduction in a single signaling pathway, via the mechanosensitive transcriptional regulators YAP and TAZ. We show that YAP and TAZ spatially couple osteoblast precursor mobilization to angiogenesis, regulate vascular loop morphogenesis to control growth plate remodeling, and mediate mechanoregulation of load-induced osteogenesis in embryonic bone. Mechanistically, YAP and TAZ uniquely regulate a subset of osteoblast-lineage cells, identified by single-cell RNA sequencing as vessel-associated osteoblast precursors. Among these cells, YAP and TAZ regulate expression of the angiogenic chemokine, Cxcl12. Functionally, in 3D human cell co-culture, CXCL12 treatment rescued angiogenesis impaired by stromal cell YAP/TAZ depletion. Together, these data establish new functions of the vessel-associated osteoblast precursors in endochondral bone development.
2023-11-15 | GSE227818 | GEO
Project description:Several transcription factors are known to be expressed in discrete regions of the otic vesicle and Dlx5 is one of those that is expressed highly in the presumptive dorsal vestibular region. Mice lacking Dlx5 have vestibular defects. Specifically, they fail to form the endolymphatic duct (a defect visible as early as E10) as well as the anterior and posterior semi-circular canals. The lateral canal does form but is smaller, whereas the saccule, the utricle and the cochlea appear relatively normal. The goal of this study was to use microarrays to identify differentially expressed genes between wild-type and Dlx5-null otic vesicles microdissected from E10 and 10.5 and identify downstream targets of Dlx5 by searching the immediate 3kb promoter regions of the differentially expressed genes for homeodomain binding sites followed by chromatin immunoprecipitation in an otic vesicle-derived cell line over-expressing Dlx5. Normal vestibular morphogenesis is compromised in mice lacking Dlx5, a member of the Distal-less family of homeobox transcription factors. We identified its direct downstream targets in the developing mouse inner ear by gene expression profiling wild-type and Dlx5 null otic vesicles from embryonic stages E10 and E10.5. Four hundred genes were differentially expressed in mutants when compared to wild-type in at least one of the two stages. To further constrain the list of likely direct targets of Dlx5, we examined the genomic DNA sequences in the 3kb promoter regions immediately proximal to the transcriptional start sites of these genes. We searched for (i) one or more previously described binding site for Dlx5, (ii) one or more novel 12bp-long motifs with a canonical homeodomain response element (HDRE) shared by promoters of two or more genes, and (iii) 100% conservation of the 12bp-long HDRE-containing motifs in promoter regions of human orthologs. Forty genes passed one or more of these filters, 12 of which are known to be expressed in the developing otic vesicle in domains that at least partially overlap with that of Dlx5 in one or both stages that we examined. Chromatin immunoprecipitation using a Dlx5 antibody confirmed direct binding of Dlx5 to promoter regions of seven of these genes (Atbf1, Bmper, Large, Lrrtm1, and Msx1, all of which were down-regulated in mutants, and Ebf1 and Lhx1, both of which were up-regulated in mutants) in an otic vesicle-derived cell line over-expressing Dlx5. Gene expression profiling of this cell line showed that Bmper and Lrrtm1 transcripts were up-regulated, further supporting their identification as direct targets of Dlx5 activity.
2011-07-01 | GSE22381 | GEO