Transcriptomic analysis of lungs with mesnchyme-specific deletion of Sin3a transcriptional regulator
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ABSTRACT:
PROVIDER: PRJNA1032475 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26535549_1.fastq.gz | Fastqsanger.gz | |||
| SRR26535549_2.fastq.gz | Fastqsanger.gz | |||
| SRR26535550_1.fastq.gz | Fastqsanger.gz | |||
| SRR26535550_2.fastq.gz | Fastqsanger.gz | |||
| SRR26535551_1.fastq.gz | Fastqsanger.gz |
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Project description:Congenital diaphragmatic hernia (CDH) is a common and severe congential malformation characterized by defects in diaphragm, lung, and pulmonary vascular developent. Despite the frequency and severity of CDH, the underlying developmental mechanisms are not understood. We identified SIN3A loss of function sequence variants in two patients with CDH. To understand the genetic and developmental mechanisms of CDH, we generated Sin3a conditional knockout mice that lack Sin3a expression in the lung mesenchyme. SIN3A plays a critcal role during development, directing cell lineage specification and cell cycling. Despite this role, SIN3A sequence variants have not been reported in patients with CDH or other congential malformations. We found that Sin3a CKO mice have abnormal lung stucture at birth into adulthood. To determine the role of Sin3a in lung mesenchymal development, we performed transcriptomic analysis of Sin3a CKO and control lungs at embryonic day 16 (E16) when cell cycling defects were first evident, postnatal day 0 (P0) when lung defects were first evident, and P3 when lung phenotyopes worsened. In this dataset are expression data from dissected embryonic and postnatal lungs of Sin3a CKO and control mice. Sin3a CKO mice have conditional deletion of Sin3a in the lung mesenchyme directed by Tbx4rtta; tetocre (Tbx4rtta; tetocre; Sin3a flox/flox CKO). Control mice are heterozygous for Sin3a in the lung mesenchyme (Tbx4rtta; tetocre; Sin3a flox/WT). These data were used to identify transcriptional changes due to loss of Sin3a in the lung mesenchyme.
2023-12-31 | GSE246305 | GEO
Project description:Congenital diaphragmatic hernia (CDH) is a common and severe congential malformation characterized by defects in diaphragm, lung, and pulmonary vascular developent. Despite the frequency and severity of CDH, the underlying developmental mechanisms are not understood. We identified SIN3A loss of function sequence variants in two patients with CDH. To understand the genetic and developmental mechanisms of CDH, we generated Sin3a conditional knockout mice that lack Sin3a expression in the lung mesenchyme. SIN3A has been shown to play a critcal role during development, directing cell lineage specification and cell cycling. We found that loss of SIN3A resulted in impaired mesenchymal cell differentiation from bulk lung transcriptomic analysis in Sin3a CKO mice. To investigate the impact of loss of SIN3A in mesenchymal cell differentation, we performed fluorescent activated cell sorting (FACS) to isolate cells that underwent recombination of Sin3a. We then performed single-cell transcriptomic analysis on sorted mesenchymal cells from embryonic day 16 (E16) Sin3a CKO and control lungs. In this dataset are expression data from FACS-isolated recombined lung mesenchymal cells of Sin3a CKO and control mice. Sin3a CKO mice have conditional deletion of Sin3a in the lung mesenchyme directed by Tbx4rtta; tetocre (Tbx4rtta; tetocre; Sin3a flox/flox CKO). Control mice are heterozygous for Sin3a in the lung mesenchyme (Tbx4rtta; tetocre; Sin3a flox/WT). These data were used to identify transcriptional changes due to loss of Sin3a in the lung mesenchyme.
2023-12-31 | GSE246194 | GEO
Project description:Congenital diaphragmatic hernia (CDH) is a common and severe congential malformation characterized by defects in diaphragm, lung, and pulmonary vascular developent. Despite the frequency and severity of CDH, the underlying developmental mechanisms are not understood. We identified SIN3A loss of function sequence variants in two patients with CDH. To understand the genetic and developmental mechanisms of CDH, we generated Sin3a conditional knockout mice that lack Sin3a expression in the lung mesenchyme. SIN3A has been shown to play a critcal role during development, directing cell lineage specification and cell cycling. We found mesenchymal progenitor cells in Sin3a CKO mice have altered expression of cell cycle progression genes from bulk lung transcriptomic analysis. To investigate changes in gene expression that occur specifically in lung mesenchymal cells, we performed fluorescent activated cell sorting (FACS) to isolate cells that underwent recombination of Sin3a. We then performed transcriptomic analysis on sorted mesenchymal cells from embryonic day 16 (E16) Sin3a CKO and control lungs. In this dataset are expression data from FACS-isolated recombined lung mesenchymal cells of Sin3a CKO and control mice. Sin3a CKO mice have conditional deletion of Sin3a in the lung mesenchyme directed by Tbx4rtta; tetocre (Tbx4rtta; tetocre; Sin3a flox/flox CKO). Control mice are heterozygous for Sin3a in the lung mesenchyme (Tbx4rtta; tetocre; Sin3a flox/WT). These data were used to identify transcriptional changes due to loss of Sin3a in the lung mesenchyme.
2023-12-31 | GSE246184 | GEO
Project description:Single-cell transcriptomic analysis of lung mesenchymal cells with mesenchyme-specific deletion of transcriptional regulator Sin3a
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Project description:Foxp3 (forkhead box protein 3) functions as the master transcriptional regulator of Treg phenotype. Histone deacetylases 1 and 2 (HDAC1/2) contribute to the regulation of FoxP3 expression via interactions with a myriad of co-regulatory factors. While the nuclear scaffolding protein, Sin3a, has been well established as a co-factor of HDAC1/2, its role within FoxP3+ Tregs has not been. We analyzed the effects of conditional deletion of Sin3a in Foxp3+ Treg cells using three orthogonal approaches. Deletion of Sin3a from FoxP3+ Tregs resulted in the rapid onset of severe and fatal autoimmunity mirroring the phenotype of Scurfy mice. Numbers of Tregs were greatly reduced, residual Tregs had virtually complete loss of suppressive function, and inducible Treg production was blocked. Mice also showed activation of effector T cells, autoantibody production and widespread tissue injury. Mechanistically, Sin3a deletion resulted in decreased transcription of Foxp3 and other Treg signature genes. The reduction of Foxp3 expression was accompanied by the reduction of TET1 and 3 expression and a complete lack of CpG demethylation of the Foxp3 enhancer region CNS2. In addition, Foxp3 protein stability was impaired and fate mapping studies showed conversion of Tregs to ex-Tregs and increased rates of programmed cell death. Thus, Sin3a plays a critical role in the maintenance of Treg identity and function and is essential for the expression and stability of Foxp3.
2024-06-07 | GSE263830 | GEO
Project description:Lung mesenchymal cells with lung-mesenchyme specific deletion of Sin3a
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Project description:Transcriptomic analysis of lung mesenchymal cells with lung-mesenchyme specific deletion of Sin3a
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Project description:Chromatin modifier Swi-independent 3a (SIN3A), together with associated histone deacetylases, influences gene expression during development and differentiation through multiple transcription factors in a cell-specific manner. Sin3a is essential for the maintenance of inner cell mass cells of mouse blastocysts, embryonic fibroblasts, and myoblasts, but is not required for the survival of trophectoderm or Sertoli cells. To better understand how this transcriptional regulator modulates cells at different developmental stages within a single lineage, we used conditional gene targeting in mice to ablate Sin3a from perinatal quiescent male gonocytes and from postnatal differentiating spermatogonia. Gene expression in the whole testes of age-matched Ddx4(Vasa/Mvh)-cre mediated conditional Sin3a gene-targeted(VSKO) mice, germ cell-specific Sin3a hemizygous (HEMI) mice, and wild type (WT) mice was measured at postnatal day 0. Two biological replicate animals were used for each condition.
2012-10-01 | E-GEOD-38096 | biostudies-arrayexpress
Project description:ChIP coupled with NGS identifies genome-wide binding sites of a ES cells specific Sin3a/Hdac complex. The aim of these experiments is to study the role of Fam60a in the Sin3a/Hdac complex. ChIP-Seq experiments reveal that Fam60a is required to maintain high levels of Sin3a binding on target genes in mESCs. Depletion of Fam60a causes a drop of Sin3a binding to target sites. Underlining the function of Fam60a in mES cells, ChIP-seq analysis of Sin3a and Fam60a in mouse fibroblasts reveal strikingly low global binding level of Sin3a to its target genes while Fam60a is absent at these sites.
2017-04-24 | GSE81081 | GEO
Project description:Chromatin modifier Swi-independent 3a (SIN3A), together with associated histone deacetylases, influences gene expression during development and differentiation through multiple transcription factors in a cell-specific manner. Sin3a is essential for the maintenance of inner cell mass cells of mouse blastocysts, embryonic fibroblasts, and myoblasts, but is not required for the survival of trophectoderm or Sertoli cells. To better understand how this transcriptional regulator modulates cells at different developmental stages within a single lineage, we used conditional gene targeting in mice to ablate Sin3a from perinatal quiescent male gonocytes and from postnatal differentiating spermatogonia.
2012-10-01 | GSE38096 | GEO