Transcriptome sequencing of E14.5 fetal liver erythroblast stage 1 cells in WT and LDB1 conditional KO mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE247801 | GEO | 2026/03/02
REPOSITORIES: GEO
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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
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Project description:Carbonic anhydrase 1 (Car1), an early specific marker of the erythroid differentiation, has been used to distinguish fetal and adult erythroid cells since its production closely follows the γ- to β-globin transition, but the molecular mechanism underlying transcriptional regulation of Car1 is unclear. Here, we show that Car1 mRNA decreases significantly when erythroid differentiation is induced in MEL cells. The Ldb1 protein complex including GATA1/SCL/LMO2 binds to the Car1 promoter in uninduced cells and reduced enrichment of the complex during differentiation correlates with loss of Car1 expression. Knockdown of Ldb1 results in a reduction of Ser2 phosphorylated RNA Pol II and Cdk9 at the Car1 promoter region, suggesting that Ldb1 is required for recruitment of Pol II as well as the transcription regulator P-TEFb to enhance elongation of Car1 transcripts. Taken together, these data show that Ldb1 forms a regulatory complex to maintain Car1 expression in erythroid cells. Expression analysis of induced and uninduced MEL cells after control or Ldb1 shRNA knockdown.
2012-12-11 | E-GEOD-42839 | biostudies-arrayexpress
Project description:Transcriptome sequencing of E14.5 fetal liver erythroblast stage 1 cells in WT and LDB1 conditional KO mice
| PRJNA1040743 | ENA
Project description:Carbonic anhydrase 1 (Car1), an early specific marker of the erythroid differentiation, has been used to distinguish fetal and adult erythroid cells since its production closely follows the γ- to β-globin transition, but the molecular mechanism underlying transcriptional regulation of Car1 is unclear. Here, we show that Car1 mRNA decreases significantly when erythroid differentiation is induced in MEL cells. The Ldb1 protein complex including GATA1/SCL/LMO2 binds to the Car1 promoter in uninduced cells and reduced enrichment of the complex during differentiation correlates with loss of Car1 expression. Knockdown of Ldb1 results in a reduction of Ser2 phosphorylated RNA Pol II and Cdk9 at the Car1 promoter region, suggesting that Ldb1 is required for recruitment of Pol II as well as the transcription regulator P-TEFb to enhance elongation of Car1 transcripts. Taken together, these data show that Ldb1 forms a regulatory complex to maintain Car1 expression in erythroid cells.
2012-12-11 | GSE42839 | GEO
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
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Project description:Many questions remain about how close association of genes and distant enhancers occurs and how this is linked to transcription activation. In erythroid cells, LDB1 is recruited to the β-globin locus via LMO2 and is required for looping of the β-globin locus control region (LCR) to the active β-globin promoter. We show that the LDB1 dimerization domain (DD) is necessary and, when fused to LMO2 is sufficient, to completely restore LCR-promoter looping and transcription in LDB1 depleted cells. The looping function of the DD is unique and irreplaceable by heterologous dimerization domains. Dissection of the DD revealed distinct functional properties of conserved subdomains. Notably, a conserved helical region (DD4/5) is dispensable for LDB1 dimerization and chromatin looping but essential for transcriptional activation. DD4/5 is required for the recruitment of the co-regulators FOG1 and NuRD complex. Lack of DD4/5 alters histone acetylation and RNA polymerase II recruitment and results in failure of the locus to migrate to the nuclear interior as normally occurs during erythroid maturation. These results uncouple enhancer-promoter looping from nuclear migration and transcription activation and reveal new roles for LDB1in these processes. RNA-seq in LDB1 knockdown, LDB1 delta4/5 construct, LDB1 full-length construct, and control in induced MEL cells; three replicates each.
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Project description:Transcriptional enhancers are brought into proximity with promoters via chromatin looping. The architectural transcription cofactor LDB1 facilitates spatial connectivity among enhancers and promoters, but whether this occurs through simple dimerization or requires heterotypic protein assemblies is unknown. Here we investigated single-stranded DNA binding proteins (SSBPs) in regulating LDB1-mediated chromatin looping and transcription. SSBP2, SSBP3, and SSBP4 colocalize with LDB1 genome-wide. Among these, only SSBP3 is essential for murine erythroid cell viability, LDB1 function, and transcription. LDB1 but not single-stranded DNA is the predominant genome-wide tether of SSBP3 to chromatin. SSBP3 depletion in SSBP2/4 knockout cells globally weakened LDB1-dependent chromatin loops and lowered nascent transcription without impacting LDB1's chromatin binding. Chromatin tethering experiments revealed SSBP3 and LDB1 mutually depend on each other to form looped contacts. SSBP3 stabilizes LDB1 dimerization in vitro, providing a possible mechanism. SSBPs emerge as key functional components of the architectural LDB1 complex.
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Project description:Transcriptional enhancers are brought into proximity with promoters via chromatin looping. The architectural transcription cofactor LDB1 facilitates spatial connectivity among enhancers and promoters, but whether this occurs through simple dimerization or requires heterotypic protein assemblies is unknown. Here we investigated single-stranded DNA binding proteins (SSBPs) in regulating LDB1-mediated chromatin looping and transcription. SSBP2, SSBP3, and SSBP4 colocalize with LDB1 genome-wide. Among these, only SSBP3 is essential for murine erythroid cell viability, LDB1 function, and transcription. LDB1 but not single-stranded DNA is the predominant genome-wide tether of SSBP3 to chromatin. SSBP3 depletion in SSBP2/4 knockout cells globally weakened LDB1-dependent chromatin loops and lowered nascent transcription without impacting LDB1's chromatin binding. Chromatin tethering experiments revealed SSBP3 and LDB1 mutually depend on each other to form looped contacts. SSBP3 stabilizes LDB1 dimerization in vitro, providing a possible mechanism. SSBPs emerge as key functional components of the architectural LDB1 complex.
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Project description:Transcriptional enhancers are brought into proximity with promoters via chromatin looping. The architectural transcription cofactor LDB1 facilitates spatial connectivity among enhancers and promoters, but whether this occurs through simple dimerization or requires heterotypic protein assemblies is unknown. Here we investigated single-stranded DNA binding proteins (SSBPs) in regulating LDB1-mediated chromatin looping and transcription. SSBP2, SSBP3, and SSBP4 colocalize with LDB1 genome-wide. Among these, only SSBP3 is essential for murine erythroid cell viability, LDB1 function, and transcription. LDB1 but not single-stranded DNA is the predominant genome-wide tether of SSBP3 to chromatin. SSBP3 depletion in SSBP2/4 knockout cells globally weakened LDB1-dependent chromatin loops and lowered nascent transcription without impacting LDB1's chromatin binding. Chromatin tethering experiments revealed SSBP3 and LDB1 mutually depend on each other to form looped contacts. SSBP3 stabilizes LDB1 dimerization in vitro, providing a possible mechanism. SSBPs emerge as key functional components of the architectural LDB1 complex.
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