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

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

PROVIDER: PRJNA757409 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15598368_1.fastq.gz	Fastqsanger.gz
	SRR15598368_2.fastq.gz	Fastqsanger.gz
	SRR15598369_1.fastq.gz	Fastqsanger.gz
	SRR15598369_2.fastq.gz	Fastqsanger.gz
	SRR15598370_1.fastq.gz	Fastqsanger.gz

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

Project description:Bulk RNA-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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