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Bulk RNA-Seq of Foxe1KO and control Nkx2-1/mKO2+ mouse ESC-derived cells

ABSTRACT: Bulk RNA-Seq of Foxe1KO and control Nkx2-1/mKO2+ mouse ESC-derived cells

PROVIDER: PRJNA756366 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15530500_1.fastq.gz	Fastqsanger.gz
	SRR15530500_2.fastq.gz	Fastqsanger.gz
	SRR15530501_1.fastq.gz	Fastqsanger.gz
	SRR15530501_2.fastq.gz	Fastqsanger.gz
	SRR15530502_1.fastq.gz	Fastqsanger.gz

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Bulk ATAC-seq of Foxe1KO and control Nkx2-1/mKO2+ mouse ESC-derived cells

Project description:Bulk ATAC-seq of Foxe1KO and control Nkx2-1/mKO2+ mouse ESC-derived cells

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Bulk ATAC-seq of Foxe1KO and control Nkx2-1/mKO2+ mouse ESC-derived cells

Project description:Functional thyroid follicles generation in vitro is obtained at high efficiency by doxycycline-mediated expression of Nkx2-1 and Pax8, two proteins involved in early specification of thyroid lineage. Although those factors are sufficient to induce thyroid specification in vitro, other players, such as Foxe1, are also present in early thyroid primordium and its loss-of-function is responsible for thyroid congenital defects in mice and humans. Here we show that Foxe1KO mESCs can be induced to differentiate towards thyroid lineage but the efficiency of thyroid follicular cells generated is drastically low. Moreover, correct expression of maturation genes and capacity to produce thyroid hormone in vitro are completely disrupted. On the other hand, Nkx2-1 expressing cells derived from Foxe1KO have an unexpected ability to deviate to a lung epithelium differentiation program and form organoids containing multiple lung cell types. These findings demonstrate that Foxe1 is required to reinforce thyroid cell fate in vitro and to promote terminal maturation of thyroid follicles.

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Bulk RNA-Seq of Foxe1KO and control Nkx2-1/mKO2+ mouse ESC-derived cells

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Subcellular proteomics of murine ESC-derived neurons

Project description:We studied the effects of different stimuli on on the subcellular proteome of neurons differentiated from murine embryonic stem cells (ESC). We focused on the changes in the chromatin-bound fraction to elucidate specific differences in the gene regulatory machinery activated upon stimulation with Brain-derived neurotrophic factor (BDNF) or a general membrane-depolarization stimulus, potassium chloride (KCl).

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PRDM3/16 Regulate Chromatin Accessibility Required for NKX2-1 Mediated Alveolar Epithelial Differentiations and Function [bulk RNA-seq]

Project description:Differential chromatin accessibility accompanies and mediates transcriptional control of diverse cell fates and their differentiation during embryogenesis. While the critical role of NKX2-1 and its transcriptional targets in lung morphogenesis and pulmonary epithelial cell differentiation is increasingly known, mechanisms by which chromatin accessibility alters the epigenetic landscape and how NKX2-1 interacts with other co-activators required for alveolar epithelial cell differentiation and function are not well understood. Here, we demonstrate that the paired domain zinc finger transcriptional regulators PRDM3 and PRDM16 regulate chromatin accessibility to mediate cell differentiation decisions during lung morphogenesis. Combined deletion of Prdm3 and Prdm16 in early lung endoderm caused perinatal lethality due to respiratory failure from loss of AT2 cell function. Prdm3/16 deletion led to the accumulation of partially differentiated AT1 cells and loss of AT2 cells. A combination of single cell RNA-seq, bulk ATAC-seq, and CUT&RUN demonstrated that PRDM3 and PRDM16 enhanced chromatin accessibility at NKX2-1 transcriptional targets in peripheral epithelial cells, with all three factors binding together at a multitude of cell-type specific cis-active DNA elements. Network analysis demonstrated that PRDM3/16 regulated genes critical for perinatal AT2 cell differentiation, surfactant homeostasis, and innate host defense. Lineage specific deletion of PRDM3/16 in AT2 cells led to lineage infidelity, with PRDM3/16 null cells acquiring a partial AT1 fate. Together, these data demonstrate that NKX2-1-dependent regulation of alveolar epithelial cell differentiations is mediated by epigenetic modulation via PRDM3/16.

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Comparison of ESC-derived and Primary-derived Tip-like Cell Transplants

Project description:The goal of this experiment was to determine whether transcriptionally similar ESC-derived and primary donor cells give rise to similar donor-derived cells following transplantation into bleomycin injured lungs.

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