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Genome binding/occuoancy profiling by high throughout sequencing in Wild Type and ID1/3 double knockout hESCs

ABSTRACT: TCF3 belongs to E protein family and has the function of transcription factor. TCF3 can directly interact with HLH family proteins ID1 and ID3 to play biological functions. ID1 and ID3 do not have the ability to directly bind to DNA and need to be regulated by TCF3. We found changes in pluripotency in ID1 and ID3 double knockout lines of human ESC, so we suspected that ID1 / 3 played a regulatory role through TCF3. Therefore, TCF3 ChIP-seq was done in WT and KO lines, hoping to find the downstream genes regulated by ID1 / 3 through TCF3, and then regulate hESC pluripotency through these genes.

ORGANISM(S): Homo sapiens

PROVIDER: GSE183518 | GEO | 2022/06/27

REPOSITORIES: GEO

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Gene expression profiles of mouse embryonic stem cells (mESCs) after genetic depletion of Id1 and knock-down of Zrf1

Project description:Id proteins are dominant negative regulators within the HLH family of proteins. In embryonic stem cells (ESCs), Id1 and Id3 maintain the pluripotent state by preventing neural differentiation. The Id1-interacting protein Zrf1 plays a crucial role as a chromatin-bound factor in specification of the neural fate from ESCs. Here, we show that Id1 blocks Zrf1 recruitment to chromatin, thus preventing the activation of neural genes during ESC differentiation. Moreover, genetic deletion of Id1 in ESCs caused misexpression of more than 6000 genes. Interestingly, the expression of almost half of those genes was restored upon further depletion of Zrf1. We therefore identified Zrf1 as a transcriptional regulator downstream of Id1 in ESCs. In Id1KO mESCs, Zrf1 expression was depleted by using shRNAs. Four replicates corresponding to four independent biological samples per group were collected.

2014-11-05 | E-GEOD-58627 | biostudies-arrayexpress

Gene expression profiles of mouse embryonic stem cells (mESCs) after genetic depletion of Id1 and knock-down of Zrf1

2014-11-05 | GSE58627 | GEO

ID1 and CEBPA coordinate epidermal progenitor cell

Project description:The regulatory circuits that coordinate epidermal differentiation during development are still not fully understood. Here we report that the transcriptional regulator ID1 is enriched in basal epidermal progenitor cells and find ID1 expression to be diminished upon differentiation. In utero silencing of Id1 impairs progenitor cell proliferation, leads to precocious delamination of targeted progenitor cells and enables differentiated keratinocytes to retain progenitor markers and characteristics. Transcriptional profiling suggests ID1 acts by mediating adhesion to the basement membrane while inhibiting spinous layer differentiation. Co-immunoprecipitation reveals ID1 binding to transcriptional regulators of the class I bHLH family. We localize bHLH Tcf3, Tcf4 and Tcf12 to epidermal progenitor cells during epidermal stratification and established TCF3 as a downstream effector of ID1-mediated epidermal proliferation. Finally, we identify crosstalk between CEBPA, a known mediator of epidermal differentiation, and Id1 and demonstrate that CEBPA antagonizes BMP-induced activation of Id1. Our work establishes ID1 as a key coordinator of epidermal development, acting to balance progenitor proliferation with differentiation and unveils how functional crosstalk between CEBPA and Id1 orchestrates epidermal lineage progression.

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Transcriptomic profiling of 4T1 cells depleted for Id1/3 and Robo1

Project description:Id1 and its closely related family member Id3 are expressed by a diversity of stem and progenitor cells. We show that Id1/3 are required for the self-renewal and proliferation of triple negative breast cancer (TNBC) cells both in vitro and in vivo. Furthermore, we identified that Id1/3 negatively regulates the tumour suppressor gene Robo1. Depletion of Robo1 could rescue the proliferative defect induced by Id1/3 knockdown. To understand the mechanisms by which Robo1 rescues cell proliferation in Id1/3 depleted cells, we performed RNA-Sequencing on 4T1 cells with Dox-inducible Id1/3 KD and/or Robo1 depletion using siRNA. We conclude that following Id1/3 knockdown, Robo1 is induced and exerts anti-proliferative effects via suppression of a Myc transcriptional program.

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Id1 and Id3 Maintain Steady State Hematopoiesis by Promoting Sinusoidal Endothelial Cell Survival and Regeneration

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Developmental ablation of Id1 and Id3 genes in the vasculature leads to postnatal cardiac phenotypes

Project description:Rationale: The Id1 and Id3 genes play major roles during cardiac development, despite their expression being confined to non-myocardial layers (endocardium – endothelium - epicardium). We previously described that Id1–/–Id3–/– double knockout (dKO) mouse embryos die at mid-gestation from multiple cardiac defects, but early demise precluded the studies of the roles of Id in the adult mice. Objective: To elucidate postnatal roles of Id genes in the heart. Methods and Results: We ablated Id1 gene in the vasculature and Id3 gene globally to generate Tie2Cre+Id1F/–Id3–/– and Tie2Cre+Id1F/FId3–/– conditional KO (Id cKO) embryos. Half of the Id cKO mice die at birth. Postnatal demise was associated with cardiac underdevelopment, enlargement, muscular ventricular septal and endothelial defects. Surviving Id cKO mice exhibited dilated, fibrotic cardiomyopathy associated with defects in the vasculature. The adult cardiac phenotype progressed into heart failure and resembled endomyocardial fibroelastosis. An abnormal vascular response was also observed in the healing process of excisional skin wounds of Id cKO mice. Expression patterns of vascular, fibrotic and hypertrophic markers were altered in the Id cKO hearts, but addition of Insulin-Like Growth Factor binding protein-3 (IGFbp3) reversed gene expression profiles of vascular and fibrotic, but not hypertrophic markers. Conclusions: Conditional ablation of Id genes in the vasculature leads to dilated fibrotic cardiomyopathy. The findings could reveal important insights into the role(s) of the endocardial network of the endothelial lineage to the development of dilated fibrotic cardiomyopathy and identify a potential therapeutic target, IGFbp3, in its treatment.

2010-10-07 | GSE21924 | GEO

Genome-wide expression profiling of 4T1 cells to identify genes that are regulated by Id1 and Id3 in breast cancer

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Transcription profiling of various cell types isolated from pancreatic islet grafts in Id1/Id3 deficient and wild type mice

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2008-06-13 | E-TABM-355 | biostudies-arrayexpress

Quantitative analysis of Id1 Wild Type and Id1 knockout hematopoietic stem cells transcriptome

Project description:To explore the molecular basis by which Id1 loss promotes HSC quiescence under stress we compared the transcriptome of Id1-/- and Id1+/+ HSCs isolated from primary BMT recipient mice by RNA-seq. We found 179 upregulated and 1476 downregulated genes in Id1-/- HSCs compared to Id1+/+ HSCs using a fold-change cut-off of 2 . Collectively, the IPA analysis shows that Id1-/- HSCs have gene expression profiles consistent with reduced response to stress, reduced cycling and proliferation, and reduced ribosomal biogenesis and protein synthesis, which is consistent with our hypothesis that Id1-/- HSCs have molecular signature of quiescent HSCs compared to Id1+/+ HSCs.

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