Ldb1 mediates trans enhancement in mammals
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA439446 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR6875220.fastq.gz | Fastqsanger.gz | |||
| SRR6875221_1.fastq.gz | Fastqsanger.gz | |||
| SRR6875221_2.fastq.gz | Fastqsanger.gz | |||
| SRR6875222.fastq.gz | Fastqsanger.gz | |||
| SRR6875223_1.fastq.gz | Fastqsanger.gz |
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Project description:LMO2 is a component of multisubunit DNA-binding transcription factor complexes that regulate gene expression in hematopoietic stem and progenitor cell development. Enforced expression of LMO2 causes leukemia by inducing hematopoietic stem cell-like features in T-cell progenitor cells, but the biochemical mechanisms of LMO2 function have not been fully elucidated. In this study we systematically dissected the LMO2/LDB1 binding interface to investigate the role of this interaction in T-cell leukemia. Alanine scanning mutagenesis of the LIM interaction domain of LDB1 revealed a discrete motif R320LITR required for LMO2 binding. Most strikingly, co-expression of full length, wild type LDB1 increased LMO2 steady state abundance, whereas co-expression of mutant proteins deficient in LMO2 binding compromised LMO2 stability. These mutant LDB1 proteins also exerted dominant negative effects on growth and transcription in diverse leukemic cell lines. Raw gene expression data on HSB-2 cells is presented here.
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Project description:How enhancers specifically connect to gene promoters is still unclear. Besides the CTCF/cohesin machinery, only a small set of nuclear factors have been studied for a direct role in physically connecting regulatory elements. Here, we show via acute degradation experiments that LDB1 directly and broadly promotes enhancer-promoter loops. Utilizing multiple degron systems, we demonstrate that most endogenous LDB1-mediated contacts can form in the absence of CTCF, cohesin and YY1. Furthermore, an engineered/forced, LDB1-driven chromatin loop can form in the absence of cohesin. Yet, in a fraction of cases cohesin driven extrusion may promote LDB1 anchored loops. Leveraging the dynamic reorganization of nuclear architecture during the transition from mitosis to G1 phase, we establish a relationship between LDB1-dependent interactions in the context of TAD organization and gene activation. Tri-C and Region Capture Micro-C reveal that LDB1 organizes multi-enhancer networks to activate transcription. This establishes LDB1 as direct driver of connectivity between regulatory elements.
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Project description:How enhancers specifically connect to gene promoters is still unclear. Besides the CTCF/cohesin machinery, only a small set of nuclear factors have been studied for a direct role in physically connecting regulatory elements. Here, we show via acute degradation experiments that LDB1 directly and broadly promotes enhancer-promoter loops. Utilizing multiple degron systems, we demonstrate that most endogenous LDB1-mediated contacts can form in the absence of CTCF, cohesin and YY1. Furthermore, an engineered/forced, LDB1-driven chromatin loop can form in the absence of cohesin. Yet, in a fraction of cases cohesin driven extrusion may promote LDB1 anchored loops. Leveraging the dynamic reorganization of nuclear architecture during the transition from mitosis to G1 phase, we establish a relationship between LDB1-dependent interactions in the context of TAD organization and gene activation. Tri-C and Region Capture Micro-C reveal that LDB1 organizes multi-enhancer networks to activate transcription. This establishes LDB1 as direct driver of connectivity between regulatory elements.
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Project description:How enhancers specifically connect to gene promoters is still unclear. Besides the CTCF/cohesin machinery, only a small set of nuclear factors have been studied for a direct role in physically connecting regulatory elements. Here, we show via acute degradation experiments that LDB1 directly and broadly promotes enhancer-promoter loops. Utilizing multiple degron systems, we demonstrate that most endogenous LDB1-mediated contacts can form in the absence of CTCF, cohesin and YY1. Furthermore, an engineered/forced, LDB1-driven chromatin loop can form in the absence of cohesin. Yet, in a fraction of cases cohesin driven extrusion may promote LDB1 anchored loops. Leveraging the dynamic reorganization of nuclear architecture during the transition from mitosis to G1 phase, we establish a relationship between LDB1-dependent interactions in the context of TAD organization and gene activation. Tri-C and Region Capture Micro-C reveal that LDB1 organizes multi-enhancer networks to activate transcription. This establishes LDB1 as direct driver of connectivity between regulatory elements.
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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.
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Project description:How enhancers specifically connect to gene promoters is still unclear. Besides the CTCF/cohesin machinery, only a small set of nuclear factors have been studied for a direct role in physically connecting regulatory elements. Here, we show via acute degradation experiments that LDB1 directly and broadly promotes enhancer-promoter loops. Utilizing multiple degron systems, we demonstrate that most endogenous LDB1-mediated contacts can form in the absence of CTCF, cohesin and YY1. Furthermore, an engineered/forced, LDB1-driven chromatin loop can form in the absence of cohesin. Yet, in a fraction of cases cohesin driven extrusion may promote LDB1 anchored loops. Leveraging the dynamic reorganization of nuclear architecture during the transition from mitosis to G1 phase, we establish a relationship between LDB1-dependent interactions in the context of TAD organization and gene activation. Tri-C and Region Capture Micro-C reveal that LDB1 organizes multi-enhancer networks to activate transcription. This establishes LDB1 as direct driver of connectivity between regulatory elements.
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Project description:How enhancers specifically connect to gene promoters is still unclear. Besides the CTCF/cohesin machinery, only a small set of nuclear factors have been studied for a direct role in physically connecting regulatory elements. Here, we show via acute degradation experiments that LDB1 directly and broadly promotes enhancer-promoter loops. Utilizing multiple degron systems, we demonstrate that most endogenous LDB1-mediated contacts can form in the absence of CTCF, cohesin and YY1. Furthermore, an engineered/forced, LDB1-driven chromatin loop can form in the absence of cohesin. Yet, in a fraction of cases cohesin driven extrusion may promote LDB1 anchored loops. Leveraging the dynamic reorganization of nuclear architecture during the transition from mitosis to G1 phase, we establish a relationship between LDB1-dependent interactions in the context of TAD organization and gene activation. Tri-C and Region Capture Micro-C reveal that LDB1 organizes multi-enhancer networks to activate transcription. This establishes LDB1 as direct driver of connectivity between regulatory elements.
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