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Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE303717 | GEO | 2026/06/20

REPOSITORIES: GEO

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Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism [ATAC-seq]

Project description:Cells and organisms can enter transient dormant states to survive unfavorable conditions during development, physiological adult states and disease. One paradigmatic case of dormancy is diapause, whereby embryos transiently pause development and enter a state of suspended animation. In mammals, diapause occurs pre-implantation at the blastocyst state and involves global growth suppression and metabolic rewiring towards lipid usage as energy source. The molecular regulation of diapause remains poorly understood, including whether it occurs by default or requires active signaling. Here, we identify the canonical TGF-β signaling pathway as an essential driver of transcriptional and metabolic reprogramming in diapause. TGF-β signaling was thought to only be required post-implantation, but we show that the ligand Nodal and its downstream effector Smad2 are essential for the survival of paused embryonic stem cells (ESCs) and blastocysts. Mechanistically, we found that Smad2 represses a Pparg, a transcription factor that is a master regulator of lipid storage, a process incompatible with pausing. Ablation of Pparg in Smad2-deficient ESCs rescues their survival and prevents excess lipid buildup in pausing conditions. These findings establish Nodal/Smad2 signaling as pivotal for sustaining embryonic diapause and suggest that the crosstalk between TGF-β signaling and the Pparg pathway may be broadly relevant for metabolic rewiring in dormancy contexts.

2026-06-22 | GSE302996 | GEO

Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism [ATAC-Seq]

2026-06-22 | GSE302766 | GEO

Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism [RNA-Seq]

2026-06-22 | GSE303716 | GEO

Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism

Project description:Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism

| PRJNA1297143 | ENA

Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism [ATAC-Seq]

Project description:Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism [ATAC-Seq]

| PRJNA1292134 | ENA

Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism [ATAC-seq]

Project description:Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism [ATAC-seq]

| PRJNA1293325 | ENA

Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism [RNA-Seq]

Project description:Nodal/Smad2 signaling sustains developmental pausing by repressing Pparg -mediated lipid metabolism [RNA-Seq]

| PRJNA1297148 | ENA

PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair

Project description:This SuperSeries is composed of the SubSeries listed below.

2024-07-30 | GSE269834 | GEO

Arf1-mediated lipid metabolism sustains cancer cells and its ablation induces anti-tumor immune responses in mice.

Project description: Not available

| S-EPMC6954189 | biostudies-literature

PPARg T166 phosphorylation-mediated lipid synthesis sustains the reparative function of macrophages during tissue repair [RNA-seq]

Project description:Macrophages exhibit a reparative phenotype that supports tissue repair and remodeling in response to tissue injury. However, the metabolic requirements that support this process have remained incompletely understood. Here, we showed that posttranslational modification (PTM) of peroxisome proliferator-activated receptor g (PPARg) regulated lipid synthesis in response to wound microenvironmental cues and that metabolic rewiring orchestrated the function of reparative macrophages. In injured tissues, repair signaling attenuated macrophage PPARg threonine 166 (T166) phosphorylation, which induced a partially active PPARg program with increased binding activity to the regulator regions of lipid synthesis-associated genes, thereby activating lipogenesis. The accumulated lipids served as signaling molecules, triggering signal transducer and activator of transcription 3 (STAT3)-mediated growth factor expression, and supporting the synthesis of phospholipids for the expansion of the endoplasmic reticulum (ER), which is required for the secretion of proteins. Genetic or pharmacological inhibition of PPARg T166 phosphorylation promoted the reparative function of macrophages and facilitated tissue regeneration. In summary, we identified that PPARg T166-regulated lipid biosynthesis was essential for the anabolic demands of the activation and function of macrophages and provided a rationale for therapeutic targeting of tissue repair.

2024-07-30 | GSE252899 | GEO

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