RNA-sequencing profiling of mRNAs in A549 cells with TIF1γ overexpression or TAF15 knockdown
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE210093 | GEO | 2022/10/19
REPOSITORIES: GEO
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Project description:RNA-sequencing profiling of mRNAs in A549 cells with TIF1γ overexpression or TAF15 knockdown
| PRJNA863643 | ENA
Project description:TAF15, a DNA and RNA-binding protein primarily localized in the nucleus, has been reported to be associated with the aging process and neurodegenerative diseases accompanied by cognitive decline. However, its role in regulating learning and memory remains unclear. Here, we discovered that TAF15 accumulates in the hippocampus of aged mice, and TAF15 overexpressing in hippocampal neurons led to spatial learning and memory impairments in young mice. These finding are further supported by the significant reduction of dendritic spines density and synaptic proteins level. Further studies revealed that overexpression of TAF15 is likely to reduce the number of dendritic spines by inhibiting the expression of Npas4 (among the most rapidly induced immediate-early genes) and its target gene Nptx2. Notably, the expression of Npas4 and Nptx2 in the hippocampus of aged mice is also downregulated. Additionally, we demonstrated that TAF15 binds to the core promoter of Npas4 gene and inhibits its transcription, and neuronal depolarization induces the dissociation of TAF15 from Npas4 promoter. Together, these findings uncover a direct role of TAF15 in regulating spatial learning and memory formation, which may provide new insights into aging-related cognitive deficits.
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Project description:Analysis of KLS cells purified from bone marrow of mice conditionally inactivated for TIF1γ gene. TIF1γ deletion results in multiple defects in adult hematopoiesis. Results provide insight into the role of TIF1γ in hematopoietic stem cells functions. We used microarrays to characterize the molecular mechanisms underlying the biological properties of KLS cells lacking TIF1γ
2012-06-25 | GSE22280 | GEO
Project description:Analysis of KLS cells purified from bone marrow of mice conditionally inactivated for TIF1γ gene. TIF1γ deletion results in multiple defects in adult hematopoiesis. Results provide insight into the role of TIF1γ in hematopoietic stem cells functions. We used microarrays to characterize the molecular mechanisms underlying the biological properties of KLS cells lacking TIF1γ KLS (lin-,c-kit+, Sca+) cells were purified by cell sorting
2012-06-24 | E-GEOD-22280 | biostudies-arrayexpress
Project description:Regulatory T cells are a suppressor population critical to control inflammation and maintain tissue homeostasis. The TGF-β pathway is a fundamental signal for regulatory T cell differentiation, yet the molecular determinants of how TGF-β signals regulate all these processes are not completely understood. TIF1γ promotes a noncanonical TGF-β/Smad pathway in HSC, however the role of TIF1γ in Treg function has been largely ignored. Here we show that TIF1γ deficient Tregs lose stability and acquire an effector phenotype upon an inflammatory stimulus. TIF1γ deficient Tregs gain a Th1-like Treg phenotype or become pro-inflammatory exTregs in an autoimmune model; while in a helminth infection model, Tregs lacking TIF1γ expression acquire a Th2-like phenotype. Loss of Foxp3 in TIF1γ deficient Tregs is cell-intrinsic, increases proliferation and enhances glycolytic capacity upon activation. Upon activation, TIF1g deficient Tregs upregulate a transcriptional profile associated with proliferation, T cell activation and T helper differentiation. Additionally, these cells acquire increased chromatin accessibility motifs for transcriptional regulators such as NFKb and different STATs; strongly suggestive of enhanced responsiveness to inflammatory cues. TIF1γ deficient Tregs show enhanced proliferation regardless TGF-β was present in the media or not; however, the T helper-like bias a Treg has in the absence of TIF1γ, occurs only in the absence of TGF-β signaling. Finally, we identified the beta-catenin pathway as the molecular mechanism driving both TIF1γ-dependent Treg stability and proliferation upon inflammation. Unlike any other previous reports eliminating different TGF-β molecular components in Tregs, deletion of TIF1γ severely impaired Treg function and stability upon inflammation. Altogether, our data demonstrates that TIF1γ is required for the maintenance of a suppressor phenotype and stability of Treg lymphocytes during inflammatory conditions in vivo and represents a new modulatory pathway to manipulate Treg cells for therapeutic purposes.
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Project description:Regulatory T cells are a suppressor population critical to control inflammation and maintain tissue homeostasis. The TGF-β pathway is a fundamental signal for regulatory T cell differentiation, yet the molecular determinants of how TGF-β signals regulate all these processes are not completely understood. TIF1γ promotes a noncanonical TGF-β/Smad pathway in HSC, however the role of TIF1γ in Treg function has been largely ignored. Here we show that TIF1γ deficient Tregs lose stability and acquire an effector phenotype upon an inflammatory stimulus. TIF1γ deficient Tregs gain a Th1-like Treg phenotype or become pro-inflammatory exTregs in an autoimmune model; while in a helminth infection model, Tregs lacking TIF1γ expression acquire a Th2-like phenotype. Loss of Foxp3 in TIF1γ deficient Tregs is cell-intrinsic, increases proliferation and enhances glycolytic capacity upon activation. Upon activation, TIF1g deficient Tregs upregulate a transcriptional profile associated with proliferation, T cell activation and T helper differentiation. Additionally, these cells acquire increased chromatin accessibility motifs for transcriptional regulators such as NFKb and different STATs; strongly suggestive of enhanced responsiveness to inflammatory cues. TIF1γ deficient Tregs show enhanced proliferation regardless TGF-β was present in the media or not; however, the T helper-like bias a Treg has in the absence of TIF1γ, occurs only in the absence of TGF-β signaling. Finally, we identified the beta-catenin pathway as the molecular mechanism driving both TIF1γ-dependent Treg stability and proliferation upon inflammation. Unlike any other previous reports eliminating different TGF-β molecular components in Tregs, deletion of TIF1γ severely impaired Treg function and stability upon inflammation. Altogether, our data demonstrates that TIF1γ is required for the maintenance of a suppressor phenotype and stability of Treg lymphocytes during inflammatory conditions in vivo and represents a new modulatory pathway to manipulate Treg cells for therapeutic purposes.
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Project description:TGFβ is known to be a potent inducer of EMT, a process involved in tumor invasion. TIF1γ has been reported to participate to TGFβ signaling. In order to understand the role of TIF1γ in TGFβ signaling and its requirement for EMT, we analyzed the TGFβ1 response of human mammary epithelial cell lines. A strong EMT increase was observed in TIF1γ-silenced cells after TGFβ1 treatment, whereas Smad4 inactivation completely blocked this process. In support of these observations, microarray data show that the functions of several TIF1γ target genes can be linked to EMT. As a negative regulator of Smad4, TIF1γ could be critical for the regulation of TGFβ signaling. This work highlights the molecular relationship between TIF1γ and Smad4 in TGFβ1 signaling and EMT.
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Project description:TAF15 (formerly TAFII68) is a member of the TET family of RNA and DNA binding proteins whose genes are frequently translocated in sarcomas. Consistent with a functional role in cell viability, TAF15 depletion had a growth-inhibitory effect and increased apoptosis. Interestingly, one of the genes affected by TAF15 depletion is CDKN1A/p21, a key regulator of cell cycle. Here we show that TAF15 down-regulates CDKN1A/p21 expression through a pathway involving miRNAs.
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Project description:To determine whether an accelerated aging-like phenotype occurs in hematopoiesis of young Tif1γ-/- mice (4 months old), we purified 200,000 hematopoietic stem cells (LSK: Lineage negative, Sca1+, c-Kit+) from Tif1γ-/- mice and performed high-throughput mRNA sequencing (RNA-seq). We compared this transcriptome to physiological aging by creating two other RNAseq libraries from young (4 months old) and old (20 months old) wild type mice. RNAseq study on young Tif1γ-/- mice (4 months old), young wild type mice (4 months old) and old wild type mice (20 months old).
2014-06-16 | E-GEOD-57396 | biostudies-arrayexpress
Project description:TAF15 (formerly TAFII68) is a member of the TET family of RNA and DNA binding proteins whose genes are frequently translocated in sarcomas. Consistent with a functional role in cell viability, TAF15 depletion had a growth-inhibitory effect and increased apoptosis. Interestingly, one of the genes affected by TAF15 depletion is CDKN1A/p21, a key regulator of cell cycle. Here we show that TAF15 down-regulates CDKN1A/p21 expression through a pathway involving miRNAs. We performed a gene expression profiling upon TAF15 knock down by RNA interference.Total RNAs purified from four biological replicates of HeLa GL3 luc cells transfected either with si-TAF15 or control si-LUC were hybridized to the array.
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