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Dynamic Enlargement and Mobilization of Lipid Droplets in Pluripotent Cells Coordinate Morphogenesis during Mouse Peri-implantation Development

ABSTRACT: Dynamic Enlargement and Mobilization of Lipid Droplets in Pluripotent Cells Coordinate Morphogenesis during Mouse Peri-implantation Development

PROVIDER: PRJNA694970 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13535260_1.fastq.gz	Fastqsanger.gz
	SRR13535260_2.fastq.gz	Fastqsanger.gz
	SRR13535261_1.fastq.gz	Fastqsanger.gz
	SRR13535261_2.fastq.gz	Fastqsanger.gz
	SRR13535262_1.fastq.gz	Fastqsanger.gz

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Dynamic Enlargement and Mobilization of Lipid Droplets in Pluripotent Cells Coordinate Morphogenesis during Mouse Peri-implantation Development

Project description:ESCs grown in Growth Factor-reduced Matrigel can recapitulate in vitro the morphogenesis of the epiblast tissue during peri-implantation development. We performed RNA-sequencing on wild-type (WT) and Cidea knockout (KO) mouse R1-ESCs grown under self-renewing (serum/LIF) conditions and in 3D culture conditions (i.e., 3D spheroids ) at different time-points of differentiation (24h and 48h post-induction) to help us understand the role of the lipid droplet associated factor CIDEA (Cell Death Inducing DFFA Like Effector A) in ESC biology and during the process of morphogenesis.

2022-05-16 | GSE165563 | GEO

Dynamic enlargement and mobilization of lipid droplets in pluripotent cells coordinate morphogenesis during mouse peri-implantation development.

Project description:Mammalian pre-implantation embryos accumulate substantial lipids, which are stored in lipid droplets (LDs). Despite the fundamental roles of lipids in many cellular functions, the significance of building-up LDs for the developing embryo remains unclear. Here we report that the accumulation and mobilization of LDs upon implantation are causal in the morphogenesis of the pluripotent epiblast and generation of the pro-amniotic cavity in mouse embryos, a critical step for all subsequent development. We show that the CIDEA protein, found abundantly in adipocytes, enhances lipid storage in blastocysts and pluripotent stem cells by promoting LD enlargement through fusion. The LD-stored lipids are mobilized into lysosomes at the onset of lumenogenesis, but without CIDEA are prematurely degraded by cytosolic lipases. Loss of lipid storage or inactivation of lipophagy leads to the aberrant formation of multiple cavities within disorganised epithelial structures. Thus, our study reveals an unexpected role for LDs in orchestrating tissue remodelling and uncovers underappreciated facets of lipid metabolism in peri-implantation development.

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TMEM41B is a novel regulator of autophagy and lipid mobilization

Project description:Autophagy maintains cellular homeostasis by targeting damaged organelles, pathogens or misfolded protein aggregates for lysosomal degradation. The autophagic process is initiated by the formation of autophagosomes, which can selectively enclose cargo via autophagy cargo receptors. A machinery of well-characterized autophagy-related proteins orchestrate the biogenesis of autophagosomes, however, the origin of the required membranes is incompletely understood. Here, we applied sensitized pooled CRISPR screens and identified the uncharacterized transmembrane protein TMEM41B as a novel regulator of autophagy. In the absence of TMEM41B, autophagosome biogenesis is stalled, LC3 accumulates at WIPI2- and DFCP1-positive isolation membranes, and lysosomal flux of autophagy cargo receptors and intracellular bacteria is impaired. In addition to defective autophagy, we found that TMEM41B knockout cells display significantly enlarged lipid droplets and reduced mobilization and β-oxidation of fatty acids. TMEM41B localizes to the endoplasmic reticulum (ER) and interacts with SIGMAR1, a chaperone which regulates calcium and lipid transfer at ER contact sites with mitochondria and lipid droplets. Taken together, we propose that TMEM41B is a novel regulator of autophagosome biogenesis and ER lipid mobilization.

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RNA-seq analysis of bone marrow peri-vascular stromal cells

Project description:Fate decisions of haematopoietic stem cells (HSCs) to self-renew or differentiate in response to various demands are finely tuned by specialized microenvironments called “niches” in the bone marrow. Recent studies suggest that arterioles and sinusoids accompanied with distinct stromal cells marked by nerve/glial antigen 2 (NG2) and leptin receptor (LepR), compose distinct niches regulating quiescence and proliferation of HSCs, respectively. However, it remains unknown how the distinct niche cells differentially regulate the HSC functions. Here we show that effects of cytokines regulating HSC functions are dependent on the producing cell sources. Deletion of chemokine C-X-C motif ligand 12 (CXCL12) in NG2-cre targeted cells, which exclusively overlap with Nestin-GFP (Nes-GFP)+ stromal cells associated with arterioles and sinusoids, resulted in a robust reductions of HSCs in the bone marrow and massive mobilization. Deletion of CXCL12 from arteriolar NG2+ vascular smooth muscle cells caused a significant decrease of HSCs and altered HSC location in the marrow, while CXCL12 depletion from sinusoidal LepR+ cells did not reduce HSC numbers in the bone marrow. By contrast, deletion of stem cell factor (SCF) in LepR+ cells led to significant reductions in HSC numbers whereas SCF deletion in arteriolar NG2+ cells showed no effect on HSC numbers in the marrow. These results uncover the distinct contributions of cytokines derived from perivascular cells in separate vascular niches for HSC maintenance and mobilization. We sought to obtain comprehensive understanding of differences between peri-arteriolar and peri-sinusoidal niche cells by the present RNA-seq analysis.

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Transcriptomic profile of Lin negative, LEPR positive cells of murine peri-implant fibrous tissue and peri-implant bone

Project description:To investigate the transcriptomic profile difference between LEPR cells in peri-implant fibrous tissue and peri-implant bone

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G-CSF plus AMD3100 mobilization in adult patients with beta-thalassemia results in effective mobilization of CD34+ cells with primitive signatures

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2017-04-28 | E-GEOD-70219 | biostudies-arrayexpress

Schizophrenia-related microdeletion causes progressive brain ventricle enlargement through microRNA-dependent deceleration of motile cilia beating

Project description:Progressive ventricular enlargement is one of the most reproducible and recognizable structural abnormalities in schizophrenia, and is associated with more severe symptoms and poorer clinical outcome. The mechanisms of ventricular enlargement in schizophrenia is unknown. We identified that progressive ventricular enlargement is associated with deceleration of motile cilia beating in ependymal cells lining ventricular walls in murine models of schizophrenia-associated 22q11 deletion syndrome (22q11DS). The cilia beating deficit is caused by an aberrant elevation of Drd1, which is highly enriched in the motile cilia. Haploinsufficiency of the microRNA-processing gene Dgcr8 is responsible for the Drd1 elevation in ependymal cells of 22q11DS mice, and is mediated by reduction of Drd1-targeting microRNAs miR-674-3p and miR-382-3p. Replenishing miR-674-3p or miR-382-3p in 22q11DS mice rescued the motile cilia beating abnormalities and normalized the ventricular size. Knockdown of these microRNA mimicked cilia beating and ventricular deficits. Ventricular enlargement was also caused by Crispr/cas9-mediated deletion of the Drd1 seed site for miR-674-3p/miR-382-3p. This suggests that Dgcr8-miR-674-3p/miR-382-3p-Drd1–dependent disruption of cilia motility in ependymal cells is a pathogenic event underlying schizophrenia-associated ventricular enlargement.

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