TAZ-mediated enhancement of adipogenesis in goat adipose mesenchymal stem cells induced by TNF-α
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ABSTRACT:
PROVIDER: PRJNA1172637 | ENA |
REPOSITORIES: ENA
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Project description:Obesity is a clinical condition characterised by a chronic, low-grade inflammatory state. Adipose-derived mesenchymal stem cells (ADSCs) have a multidirectional differentiation potential to adipocytes. However, the relationship between adipogenesis and inflammation is not yet fully understood.TAZ (WW domain containing transcription regulator 1) can act as a molecular rheostat to fine-tune the osteoblast and adipocyte differentiation balance. In this study, we investigated the role of TAZ in the adipogenesis of Arbas cashmere goat ADSCs (gADSCs). We observed elevated TAZ expression levels during the adipogenesis of gADSCs. Overexpression and knockdown of TAZ were performed in stably transfected gADSCs cell lines, and RNA-seq analysis revealed that TAZ was associated with adipogenesis. TAZ overexpression promoted adipose differentiation of gADSCs, while TAZ knockdown had the opposite effect. In addition, TAZ overexpression and knockdown altered the expression of YAP1 (Yes1 associated transcriptional regulator) and TAZ in the nucleus. TAZ regulated the mRNA expression level and secretion level of tumor necrosis factor (TNF)-α, promoting adipose differentiation of gADSCs. Notably, TNF-α counteracted the inhibitory effect of sh-TAZ on the adipose differentiation of gADSCs. Collectively, these findings suggest that TAZ regulates adipogenesis in gADSCs by modulating TNF-α, which is of particular significance in several metabolic disorders where the amount or function of adipose tissue is altered.
2024-10-17 | GSE279395 | GEO
Project description:Protein kinase A phosphorylates proteins including histone H3 lysine 9 (H3K9) demethylase JMJD1A to facilitate beige adipogenesis upon β-adrenergic receptor (β-AR) activation, however, phosphatase(s) that antagonizes phosphorylation to inhibit beige adipogenesis is incompletely understood. Here we show that MYPT1-PP1β is a phosphatase that negatively regulates beige adipogenesis via dephosphorylation of pS265-JMJD1A and myosin regulatory light chain. Upon β-AR activation, MYPT1-PP1β is inhibited via T694 phosphorylation of MYPT1, facilitating phosphorylation of JMJD1A and beige adipogenesis under cold stress. Depletion of MYPT1-PP1β induces Ucp1 by orchestrating JMJD1A-mediated H3K9 demethylation and actomyosin-tension mediated YAP/TAZ activation. This induction of Ucp1 is abrogated in adipocytes expressing catalytically dead JMJD1A mutant, indicating that the coordinated epigenetic and transcriptional mechanisms are essential for beige adipogenesis. We also show that preadipocytes specific Mypt1 deficient mice exhibit higher cold tolerance with higher Ucp1 levels in subcutaneous white adipose tissues compared to control mice confirming its role at animal levels.
2022-09-26 | PXD031210 | JPOST Repository
Project description:mRNA sequencing of mesenchymal stem cells transfected with YAP/TAZ siRNAs were treated with or without TNF-a for 24hr to profile gene expressions.
2023-10-30 | GSE246340 | GEO
Project description:Local breeds retained unique genetic variability important for adaptive potential especially in light of challenges related to climate change. Our objective was to perform, for the first time, a genome-wide diversity characterization using Illumina GoatSNP50 BeadChip of autochthonous Drežnica goat breed from Slovenia. Genetic diversity analyses revealed that the Slovenian Drežnica goat has a distinct genetic identity and is closely related to the neighboring Austrian and Italian alpine breeds. These results expand our knowledge on phylogeny of goat breeds from easternmost part of the European Alps.
2021-06-05 | GSE176157 | GEO
Project description:We demonstrated that TAZ positively regulates Irs1 gene transcription in muscle. Therefore we designed ChIP-seq experiment to reveal detailed mechanism of regulation. To capture TAZ in chromatin preparation, we made Flag-tagged TAZ expressing and control vector transduced C2C12 cells by retroviral infection. We used FLAG-conjugated beads to capture TAZ-chromatin complexes and ChIP-seq was perforemd. Among many TAZ binding sites, we focused Irs1 regulatory region because our primary purpose was to identify TAZ binding site for the regulation of Irs1 transcription.
2018-12-13 | E-MTAB-6764 | biostudies-arrayexpress
Project description:The present study, for the first time, compared the transcriptomes of ovaries from the prolific Jintang black goat and the non-prolific Tibetan goat during follicular phase using the Illumina RNA-Seq method. The study provides insight into the transcriptional regulation in the ovaries of two distinct breeds of goats that might serve as a key resource for understanding goat fecundity.
2017-11-22 | GSE87878 | GEO
Project description:The optic vesicle comprises a pool of bi-potential progenitor cells from which the retinal pigment epithelium (RPE) and neural retina fates segregate during ocular morphogenesis. Several transcription factors and signaling pathways have been shown to be important for RPE maintenance and differentiation, but an understanding of the initial fate specification and determination of this ocular cell type is lacking. We show that Yap/Taz-Tead activity is necessary and sufficient for optic vesicle progenitors to adopt RPE identity in zebrafish. A Teadresponsive transgene is expressed within the domain of the optic cup from which RPE arises, and Yap immunoreactivity localizes to the nuclei of prospective RPE cells. yap (yap1) mutants lack a subset of RPE cells and/or exhibit coloboma. Loss of RPE in yap mutants is exacerbated in combination with taz (wwtr1) mutant alleles such that, when Yap and Taz are both absent, optic vesicle progenitor cells completely lose their ability to form RPE. The mechanism of Yap dependent RPE cell type determination is reliant on both nuclear localization of Yap and interaction with a Tead co-factor. In contrast to loss of Yap and Taz, overexpression of either protein within optic vesicle progenitors leads to ectopic pigmentation in a dosagedependent manner. Overall, this study identifies Yap and Taz as key early regulators of RPE genesis and provides a mechanistic framework for understanding the congenital ocular defects of Sveinsson’s chorioretinal atrophy and congenital retinal coloboma. 60 pooled eyes from 36 hpf wild type or vsx2:Gal4/dsRed:14xUAS:YapS87A embryos were pooled for one sample. Three wild type and three vsx2:Gal4/dsRed:14xUAS:YapS87A pools were analyzed for RNA.
2015-08-06 | E-GEOD-71681 | biostudies-arrayexpress
Project description:The two effector proteins of the Hippo signaling pathway, YAP and TAZ, play a pivotal role in the cellular homeostasis of podocytes and in the pathogenesis of focal segmental glomerulosclerosis (FSGS). We aim to unravel the unique and redundant functions of YAP and TAZ in the podocyte by identifying podocyte-specific interactors. We generated stable heat sensitive mouse podocytes (hsMPs) carrying a single copy integration of a transgenic construct expressing a flagged version of mouse Yap (3XFLAG.YAP), Taz (3XFLAG.TAZ) or Ruby (3XFLAG.RUBY) in the Rosa26 locus. To explore the interactome of YAP and TAZ in podocytes we immunoprecipitated the tagged proteins and characterized the co-immunoprecipitated protein complexes by mass spectrometry. Within the interactome analyses of the hsMPs, we identified shared and non-shared interacting proteins between YAP and TAZ. Among these identified proteins many well established interactors of YAP and TAZ were included, like proteins of the Tead family, different angiomotins or large tumor suppressor kinase 1 (Lats1). Strikingly, among the shared proteins were numerous proteins of the nuclear shuttling machinery, like importins (Ipo), exportins (Xpo), transportins (Tnpo) and nucleoporins (Nup) that form the nuclear pore complex (NPC), such as NUP107, NUP133, NUP205 and XPO5.
2024-01-26 | PXD040448 | Pride