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Next-generation sequencing of cTEC and mTEC isolated from non-pregnant and pregnant females lacking the expression of Klf4 (KO) or not (LOX)

ABSTRACT: Next-generation sequencing of cTEC and mTEC isolated from non-pregnant and pregnant females lacking the expression of Klf4 (KO) or not (LOX)

PROVIDER: PRJNA868101 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20998030.fastq.gz	Fastqsanger.gz
	SRR20998031.fastq.gz	Fastqsanger.gz
	SRR20998032.fastq.gz	Fastqsanger.gz
	SRR20998033.fastq.gz	Fastqsanger.gz
	SRR20998034.fastq.gz	Fastqsanger.gz

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Next-generation sequencing of cTEC and mTEC isolated from non-pregnant and pregnant females lacking the expression of Klf4 (KO) or not (LOX)

Project description:Stress-induced thymic involution is defined by profound damage to thymic epithelial cells (TECs), resulting in an acute and transient reduction of thymopoietic capacity. During pregnancy, thymic involution is not associated with TEC loss but rather with TEC quality modifications. Study of the mechanisms of TEC maintenance during pregnancy may be of critical importance for identifying new players for thymic regeneration in other models of thymic involution. We report a strong enrichment for motifs recognized by KLF4 based on genes differentially expressed in TECs of pregnant females. Therefore, we studied the impact of Klf4 deletion in TECs during pregnancy by analyzing thymus composition and TEC transcriptome. Conditional Klf4 deletion in homeostatic conditions does not injure thymic integrity. However, pregnant females lacking Klf4 show a disrupted thymus with substantial loss of thymic epithelial cells. Klf4 maintains cTEC number during pregnancy by maintaining cell survival and inhibiting the transition to a mesenchymal state. Our study reveals Klf4 as a protective factor for TECs during pregnancy-associated thymic involution and represents a potential study subject for other models of stress-induced thymic involution.

2022-09-30 | GSE210885 | GEO

LC-MSMS of the MHC-I immunopeptidome of murine thymic epithelial cells

Project description:Antigen presentation by cortical and medullary thymic epithelial cells (cTEC and mTEC) ensures the formation of a self-restricted and self-tolerant T cell repertoire, respectively. As such, a broad diversity of self-antigens needs to be presented by mTEC to induce T cell’s self-tolerance. Even though the expression and antigen presentation of protein coding genes in mTEC has been abundantly described, little is known of the implication of allegedly noncoding regions of the genome to tolerance induction. In this study, we focused on transposable elements (TE), which have been shown to be highly expressed by mTEC.

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Zuklys etal_TECmRNA_DicerWT_vs_KO

Project description:mTEC and cTEC profiles from 2 week old Dicer fl/fl (WT) and Foxn1Cre::Dicer fl/fl mice. cTEC(CD45-EpCAM+MHCII+UEA-1-Ly51+) and mTEC(CD45-EpCAM+MHCII+UEA-1+Ly51-) were isolated from thymus tissue by cell sorting

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Gene Expression Data from Adult and Embryo Thymic Epithelial Cells (TEC)

Project description:We used Affymetrix microarrays to understand the genome wide differences in Adult and fetal cortical thymic epithelial cells (cTEC) and medullary thymic epithelial cells (mTEC)

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Klf6 is required in thymic epithelial cells for normal thymus development [scATAC-seq]

Project description:Thymic epithelial cells (TEC) control T cell development and play essential roles in establishing self-tolerance. Transcription factors controlling TEC development are poorly characterized. We report that Klf6 plays a critical role in TEC development. Mice deficient for Klf6 in TEC had a hypoplastic thymus - evident from fetal stages into adulthood. Proliferation of TEC was not reduced, but a dramatic increase in the frequency of apoptotic TEC in fetal and adult thymus was observed. Among cortical TEC (cTEC), we found expansion of a previously unreported cTEC population expressing the transcription factor Sox10. Medullary TEC (mTEC) subsets were not equally impacted with Ccl21a+ mTEC I and Tuft-like mTEC IV being disproportionately affected. Consistent with these TEC defects, naïve conventional T cells and NKT cells were reduced in the spleen, and signs of autoimmunity were evident. Thus, Klf6 has a pro- survival role in TEC and is also required for differentiation of the mTEC I and mTEC IV populations of TEC in adult mice. In this work, we report that mice with Foxn1-Cre mediated ablation of Klf6 in TEC demonstrate thymic hypoplasia beginning from prenatal life and extending through adulthood. Guided by single-cell transcriptional profiling, we determined that loss of Klf6 increased programmed cell death of TEC in prenatal and adult mice. In adult mice, thymic Klf6 deficiency severely impacted the mTEC I and mTEC IV populations. In addition, Klf6 deficiency led to the expansion of a previously uncharacterized cTEC population expressing Sox10 that is present in wild-type mice at very low frequencies. We observed concordant reductions of the naïve αβ T cell and iNKT pools in the periphery of young adult mice. Furthermore, we detected T cell infiltration in salivary and lacrimal glands, indicating defects in T cell tolerance.

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Expression data from E11.5 mouse branchial arch 1 (BA1) - comparison between Ezh2lox/lox and Wnt1Cre Ezh2lox/lox embryos

Project description:Conditional ablation of Ezh2 in the neural crest lineage results in loss of the neural crest-derived mesenchymal derivatives. In this data sheet we determine gene expression analysis in Ezh2lox/lox and Wnt1Cre Ezh2lox/lox in E11.5 mouse BA1 cells. Conditional ablation of Ezh2 in the neural crest lineage was achieved by crossing Wnt1creEzh2lox/wt mice with Ezh2lox/lox mouse lines. We analyzed a total of 6 samples including 3 biological replicates from Ezh2lox/lox embryos and 3 biological replicates from Wnt1cre Ezh2lox/lox embryos.

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Expression data from E11.5 mouse branchial arch 1 (BA1) - comparison between Ezh2lox/lox and Wnt1Cre Ezh2lox/lox embryos

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