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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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The role of Ldb1 in hemangioblast development: genome-wide analysis shows that Ldb1 controls essential hematopoietic genes/pathways in mouse early development and reveals novel players in hematopoiesis

ABSTRACT: This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: supat thongjuea

PROVIDER: E-GEOD-43044 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Genome-wide analysis shows that Ldb1 controls essential hematopoietic genes/pathways in mouse early development and reveals novel players in hematopoiesis.

Mylona Athina A Andrieu-Soler Charlotte C Thongjuea Supat S Martella Andrea A Soler Eric E Jorna Ruud R Hou Jun J Kockx Christel C van Ijcken Wilfred W Lenhard Boris B Grosveld Frank F

Blood 20130206 15

The first site exhibiting hematopoietic activity in mammalian development is the yolk-sac blood island, which originates from the hemangioblast. Here we performed differentiation assays, as well as genome-wide molecular and functional studies in blast colony-forming cells to gain insight into the function of the essential Ldb1 factor in early primitive hematopoietic development. We show that the previously reported lack of yolk-sac hematopoiesis and vascular development in Ldb1(-/-) mouse result ...[more]

PMID: 23390196

Similar Datasets

The role of Ldb1 in hemangioblast development: genome-wide analysis shows that Ldb1 controls essential hematopoietic genes/pathways in mouse early development and reveals novel players in hematopoiesis (sequencing)

Project description:The first site exhibiting hematopoietic activity in mammalian development is the yolk sac blood island, which originates from the hemangioblast. Here we performed differentiation assays, as well as genome-wide molecular and functional studies in BL-CFCs to gain insight into the function of the essential Ldb1 factor in early primitive hematopoietic development. We show that the previously reported lack of yolk sac hematopoiesis and vascular development in Ldb1-/- mouse result from a decreased number of hemangioblasts and a block in their ability to differentiate into erythroid and endothelial progenitor cells. Transcriptome analysis and correlation with the genome wide binding pattern of Ldb1 in hemangioblasts revealed a number of direct target genes and pathways misregulated in the absence of Ldb1. The regulation of essential developmental factors by Ldb1 defines it as an upstream transcriptional regulator of hematopoietic/endothelial development. We show the complex interplay that exists between transcription factors and signaling pathways during the very early stages of hematopoietic/endothelial development and the specific signalling occurring in hemangioblasts in contrast to more advanced hematopoietic developmental stages. Finally, by revealing novel genes and pathways, not previously associated with early development, our study provides novel candidate targets to manipulate the differentiation of hematopoietic and/or endothelial cells. Examination of endogenous Ldb1 genome-wide binding sites comparsion between ChIP and Control on Flk1+ BL-CFCs RNA was isolated from Ldb1+/+ and Ldb1-/- Flk1+ cells with the QIAGEN RNeasy Mini Kit and integrity was checked on the Agilent 2100 Bioanalyzer. RNA sequencing was performed on Illumina HiSeq 2000 platform according to the manufacturer instructions.

2013-02-09 | E-GEOD-43041 | biostudies-arrayexpress

Ldb1-nucleated transcription complexes function as primary mediators of erythroid gene activation

Project description:We used ChIP-Seq to map Ldb1, Scl and Gata1 binding sites in mouse total bone marrow cells. Together with functional studies comparing gene expression in Murine Erythroleukemia (MEL) cells expressing Ldb1 shRNA or control shRNA and bioinformatics analysis, we systematically determined the transcriptional program controlled by Ldb1 complexes in erythropoiesis. This represents the ChIP-Seq component of the study only To evaluate the role of Ldb1complexes in erythroid gene activation

2013-04-29 | E-GEOD-42843 | biostudies-arrayexpress

LARP1 mRNP scaffolds mTORC1 to stimulate translation initiation of an essential class of mRNAs

Project description:The RNA biding protein, LARP1, has been proposed to function downstream of mTORC1 to positively regulate the translation of 5M-bM-^@M-^YTOP mRNAs such as ribosome protein (RP) mRNAs. However, its regulatory roles in mTORC1-mediated translation remain unclear. PAR-CLIP of LARP1 revealed its direct and dynamic interactions with RP mRNAs through pyrimidine-enriched sequences in the 5M-bM-^@M-^YUTR of RP mRNAs when mTOR activity is inhibited. Importantly, this LARP1 is a direct substrate of mTORC1 and S6K1/Akt, and phosphorylated LARP1 scaffolds mTORC1 on translation-competent mRNAs to facilitate 4EBP1 and S6K1 phosphorylation. Ablation of LARP1 causes multiple defects in the processes of translation including abnormal eIF4G1 interaction with RP mRNAs and inefficient RP mRNA elongation thereby reducing ribosome biogenesis and cell proliferation. These observations illustrate that LARP1 functions both an effector and a regulator for local mTORC1 activity, and acts as a molecular switch for ribosome biogenesis by sensing growth factor/nutrient signaling. LARP1-bound RNA regions were sequenced from HEK293T cells under growing or mTOR-inactive conditions. In parallel, mRNA abundance was quantified, in biological duplicate, from HEK293T cells under the same conditions.

2014-07-31 | E-GEOD-59599 | biostudies-arrayexpress

LIM domain binding protein 1 regulates a transcriptional program essential for hematopoietic stem cell maintenance

Project description:We used ChIP-Seq to map Ldb1, Scl and Gata2 binding sites in mouse hematopoietic progenitor cells (HPCs). Together with functional studies using conventional and conditional Ldb1 deficient mouse models and bioinformatics analysis, we systematically determined a transcriptional program controlled by Ldb1 complexes in HSC maintenance. To evaluate the role of Ldb1 in hematopoietic stem cell maintenance.

2011-01-04 | E-GEOD-26031 | biostudies-arrayexpress

The transcription factor IRF4 is essential for T cell receptor affinity mediated metabolic programming and clonal expansion of T cells [ChIP-seq]

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2013-08-17 | E-GEOD-49930 | biostudies-arrayexpress

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Project description:Humoral immunity requires the generation of high-affinity antibodies, which involves the generation of germinal centres (GC) promoting class switch and affinity maturation of antigen-specific B cells, and the differentiation of long-lived plasma cells. This multi-layered process is tightly controlled by the activity of a transcriptional network including Bcl6, essential for the development of GC, and Blimp1, required for the differentiation of plasma cells. Here, we reveal an additional layer of complexity by demonstrating that dynamic changes in E-protein activity mediated by Id3 govern both GC and plasma cell differentiation. We show that down-regulation of Id3 expression in B cells in essential for releasing E2A and E2-2, the combined activity of which is required for both GC B cell and plasma cell differentiation. We demonstrate that this pathway controls the expression of multiple key factors required for antigen-induced B cell differentiation, including Blimp1, Xbp1, Mef2b and CXCR4 and is therefore critical for establishing the transcriptional network that controls GC B cell and plasma cell differentiation. Genome binding of transcription factor E2A

2016-05-13 | E-GEOD-72828 | biostudies-arrayexpress

Distinct Global Shifts in Genomic Binding Profiles of Limb Malformation Associated HOXD13 Mutations

Project description:We applied ChIP-seq to explore the effect of missense mutations in TFs on their genome wide binding profile. Using a retroviral expression system in chicken mesenchymal stem cells, we elucidated the mechanism underlying a novel missense mutation in HOXD13 (Q317K) associated with a complex hand and foot malformation phenotype. The glutamine at position 317 (position 50 of the homeodomain) is conserved in most homeodomains, a notable exception being bicoid-type homeodomains that have K at this position. Our results show that the mutation results in a shift in the binding profile of the mutant towards a bicoid/PITX1 motif. Gene expression analysis and functional assays using in vivo overexpression studies confirm that the mutation results in a partial conversion of HOXD13 into a TF with bicoid/PITX1 properties. A similar shift was not observed with the mutation Q317R, which is associated with brachysyndactyly, suggesting that the bicoid/PITX1-shift observed for Q317K might be related to the severe clinical phenotype. For each wt or mutant transcription factor two independent biological replicates were used for ChIP-seq together with corresponding input DNA as reference samples. For expression analysis one RNA sample for each wt and mutant transcription factor was used and compared to the expression level of cells infected with empty vector by RNA-seq.

2013-08-19 | E-GEOD-44799 | biostudies-arrayexpress

Transcriptionally active chromatin channels DNA double-strand breaks to RAD51-dependent repair

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2014-03-23 | E-MTAB-1241 | biostudies-arrayexpress

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2015-05-22 | E-GEOD-68356 | biostudies-arrayexpress

ChIP-seq of ER, PR, p300 in two ER+ breast cancer cell lines treated with estrogen and with and without progestins

Project description:Exploring effect of progesterone/progestin treatment on ER and PR binding. Two cell lines, three conditions (Full Media with E2, E2+ Progesterone, Full Media + R5020 Progestin), three factors (ER, PR, p300), all with three replicates, each with a matched Input control.

2015-05-22 | E-GEOD-68355 | biostudies-arrayexpress

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