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ChIP-Seq of TAL1 and its regulatory partners in T-ALL cells

ABSTRACT: The oncogenic transcription factor TAL1/SCL is aberrantly expressed in over 40% of cases of T-cell acute lymphoblastic leukemia (T-ALL), emphasizing its importance in the molecular pathogenesis of T-ALL. Here we identify the core transcriptional regulatory circuit controlled by TAL1 and its regulatory partners HEB, E2A, LMO1, LMO2, GATA3 and RUNX1 in T-ALL cells. We show that TAL1 forms an interconnected auto-regulatory loop with its partners, and that the TAL1 complex directly activates the MYB oncogene, forming a feed-forward positive regulatory loop that further promotes the TAL1-regulated oncogenic program. one of the cirtical downstream targets in this circuitry is the TRIB2 gene, which is oppositely regulated by TAL1 and HEB/E2A, and is essential for the survival of T-ALL cells.

ORGANISM(S): Homo sapiens

PROVIDER: GSE29180 | GEO | 2012/02/09

SECONDARY ACCESSION(S): PRJNA142977

REPOSITORIES: GEO

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ChIP-Seq of TAL1 and its regulatory partners in T-ALL cells

Project description:The oncogenic transcription factor TAL1/SCL is aberrantly expressed in over 40% of cases of T-cell acute lymphoblastic leukemia (T-ALL), emphasizing its importance in the molecular pathogenesis of T-ALL. Here we identify the core transcriptional regulatory circuit controlled by TAL1 and its regulatory partners HEB, E2A, LMO1, LMO2, GATA3 and RUNX1 in T-ALL cells. We show that TAL1 forms an interconnected auto-regulatory loop with its partners, and that the TAL1 complex directly activates the MYB oncogene, forming a feed-forward positive regulatory loop that further promotes the TAL1-regulated oncogenic program. one of the cirtical downstream targets in this circuitry is the TRIB2 gene, which is oppositely regulated by TAL1 and HEB/E2A, and is essential for the survival of T-ALL cells. Human T-ALL cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total TAL1 (Santa Cruz SC-12984), TCF12/HEB (Santa Cruz SC-357),TCF3/E2A (Santa Cruz SC-349X), LMO1 (Santa Cruz SC-10494), LMO2 (R&D AF2726),GATA3 (Santa Cruz SC-22206) and RUNX1 (Santa Cruz SC-8563). This represents the ChIP-seq portion of this dataset.

2012-02-09 | E-GEOD-29180 | biostudies-arrayexpress

Identification of differentially expressed genes upon shRNA knockdown of TAL1 and its regulatory partners in T-ALL cells (Jurkat)

2012-08-16 | E-GEOD-29179 | biostudies-arrayexpress

Core transcriptional regulatory circuit controlled by the tal1 complex in human t-cell acute lymphoblastic leukemia (Subseries)

Project description:The oncogenic transcription factor TAL1/SCL is aberrantly overexpressed in over 40% of cases of T-cell acute lymphoblastic leukemia (T-ALL), emphasizing the importance of the TAL1-regulated transcriptional program in the molecular pathogenesis of T-ALL. Here we identify the core transcriptional regulatory circuit controlled by TAL1 and its regulatory partners HEB, E2A, GATA3, ETS1 and RUNX1 in T-ALL cells. We find that TAL1 forms an interconnected auto-regulatory loop with its partners, which contributes to the sustained upregulation of its direct target genes. Importantly, we also find the MYB oncogenic transcription factor is directly activated by the TAL1 complex and positively regulates many of the same target genes, thus forming a feed-forward positive regulatory loop that further promotes the TAL1-regulated oncogenic program. Human T-ALL cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total TAL1 (Santa Cruz SC-12984), TCF12/HEB (Santa Cruz SC-357),TCF3/E2A (Santa Cruz SC-349X), LMO1 (Santa Cruz SC-10494), LMO2 (R&D Systems AF2726), GATA3 (Santa Cruz SC-22206) and RUNX1 (Santa Cruz SC-8563). This represents the ChIP-seq portion of this dataset. Human Jurkat cells were cross-linked with formaldehyde for 20 min. DNA was enriched by chromatin immunoprecipitation (ChIP) and analyzed by Solexa sequencing. A sample of whole cell extract (WCE) was sequenced and used as the background to determine enrichment. ChIP was performed using an antibody against total TAL1 (Santa Cruz SC-12984), TCF12/HEB (Santa Cruz SC-357),TCF3/E2A (Santa Cruz SC-349X), LMO1 (Santa Cruz SC-10494), GATA3 (Santa Cruz SC-22206) and RUNX1 (Santa Cruz SC-8563). This represents the ChIP-seq portion of this dataset.

2012-03-14 | E-GEOD-33850 | biostudies-arrayexpress

Identification of differentially expressed genes upon shRNA knockdown of TAL1 and its regulatory partners in T-ALL cells (Jurkat)

2012-08-16 | GSE29179 | GEO

Core transcriptional regulatory circuit controlled by the tal1 complex in human t-cell acute lymphoblastic leukemia (Subseries)

2012-03-14 | GSE33850 | GEO

TAL1 complex in human T-cell acute lymphoblastic leukemia (RPMI-8402)

2012-07-09 | GSE39179 | GEO

TAL1 complex in human T-cell acute lymphoblastic leukemia (RPMI-8402)

2012-07-09 | E-GEOD-39179 | biostudies-arrayexpress

Progression from the preleukemic stage to acute leukemia in TAL1/SCL-LMO1 transgenic mice

Project description:The TAL1/SCL and LMO1 oncogenic transcription factors establish a pre-leukemic state by reprogramming thymocytes into self-renewing pre-leukemic stem cells (pre-LSCs). Pre-TCR signaling accelerates the progression to T-cell acute lymphoblastic leukemia (T-ALL). To directly address the importance of pre-TCR signaling in driving progression to T-ALL, we leverage on Cd3-deficient mice in which pre-TCR signaling and progression through β-selection is abrogated. In the absence of pre-TCR signaling in Cd3ε-deficient SCL-LMO1 transgenic mice, T-ALL onset is delayed by 150 days. Despite the absence of pre-TCR/CD3 signaling in these mice, we show that leukemic thymocytes exhibit the gene expression profiles of thymocytes that have undergone β-selection, i.e. exhibiting a re-activation of pre-TCR-driven proliferation signature, and a down regulation of HEB/TCF12 target genes. Lastly, monoallelic deletion of Heb is sufficient to accelerate T-ALL onset in Cd3ε-deficient SCL-LMO1 transgenic mice. Together, these results underscore the role of HEB/TCF12 as a tumor suppressor in T-ALL.

2022-03-27 | GSE198506 | GEO

Genes regulated by HEB and E2A during DP stage of thymocyte development

Project description:To investigate gene targets of the E-proteins HEB and E2A during the CD4+CD8+ double positive (DP) stage of T cell development. We examined E-protein function by simultaneous removal of both HEB (Tcf12) and E2A (Tcfe2a) genes at the DP stage. This was done by crossing mice containing HEB floxed and E2A floxed alleles to a CD4Cre background (Tcf12f/fTcfe2af/fCD4Cre mice). Microarray analysis was used to compare gene expression in HEB and E2A double deficient DP thymocytes (Cre+) to Cre- control DP thymocytes. Keywords: genetic modification

2007-12-04 | GSE9749 | GEO

Identification of LMO2 transcriptome and interactome in diffuse large B-cell lymphoma

Project description:LMO2 regulates gene expression facilitating the formation of multipartite DNA-binding complexes. In B cells, LMO2 is specifically up-regulated in the Germinal Center (GC) reaction and is expressed in GC-derived non-Hodgkin’s lymphomas. LMO2 is one of the most powerful prognostic indicators in DLBCL patients. However, its function in GC B cells and DLBCL is currently unknown. In the present study we characterized the LMO2 transcriptome and interactome in DLBCL cells. LMO2 regulates genes implicated in kinetochore function, chromosome assembly and mitosis. Overexpression of LMO2 in DLBCL cell lines results in centrosome amplification. In DLBCL, the LMO2 complex contains some of the traditional partners such as LDB1, E2A, HEB, Lyl1, ETO2 and SP1, but not TAL1 or GATA proteins. Furthermore, we identified novel LMO2 interacting partners: ELK1, NFATc1 and LEF-1 proteins. Reporter assays revealed that LMO2 increases transcriptional activity of NFATc1 and decreases transcriptional activity of LEF-1 proteins. Overall, our studies identified a novel LMO2 transcriptome and interactome in DLBCL and provide a platform for future elucidation of LMO2 function in GC B-cells and DLBCL pathogenesis. RCK8 DLBCL cell lines were stably transfected with control plasmid or plasmid+LMO2

2012-07-12 | E-GEOD-34576 | biostudies-arrayexpress

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