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Shroom3 Affects Neuroepithelial Morphogenesis through Regulating Cytoskeletal Proteins in Cynomolgus Monkey’s Organoids

ABSTRACT: The loss of SHROOM3 plays an important role at the neuroepithelial stage, demonstrating the indispensability of SHROOM3 and indicating the great potential of organoids in understanding the mechanism of neural tube defects (NTDs).

ORGANISM(S): Macaca fascicularis

PROVIDER: GSE217791 | GEO | 2025/11/01

REPOSITORIES: GEO

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Shroom3 Affects Neuroepithelial Morphogenesis through Regulating Cytoskeletal Proteins in Cynomolgus Monkey’s Organoids

Project description:Shroom3 Affects Neuroepithelial Morphogenesis through Regulating Cytoskeletal Proteins in Cynomolgus Monkey’s Organoids

| PRJNA900552 | ENA

Loss of SHROOM3 affects neuroepithelial cell shape through regulating cytoskeleton proteins in cynomolgus monkey organoids.

Project description: Not available

| S-EPMC11017078 | biostudies-literature

A Shared Pathogenic Mechanism for Valproic Acid and SHROOM3 Knockout in a Brain Organoid Model of Neural Tube Defects

Project description:Neural tube defects (NTDs) including anencephaly and spina bifida are common major malformations of fetal development resulting from incomplete closure of the neural tube. These conditions lead to either universal death (anencephaly) or life-long severe complications (spina bifida). Despite hundreds of genetic mouse models having neural tube defect phenotypes, the genetics of human NTDs are poorly understood. Furthermore, pharmaceuticals such as antiseizure medications have been found clinically to increase the risk of NTDs when administered during pregnancy. Therefore, a model that recapitulates human neurodevelopment would be of immense benefit to understand the genetics underlying NTDs and identify teratogenic mechanisms. Using our self-organizing single rosette spheroid (SOSRS) brain organoid system, we have developed a high-throughput image analysis pipeline for evaluating SOSRS structure for NTD-like phenotypes. Similar to small molecule inhibition of apical constriction, the antiseizure medication valproic acid (VPA), a known cause of NTDs, increases the apical lumen size and apical cell surface area in a dose-responsive manner. This expansion was mimicked by GSK3b and HDAC inhibitors; however, RNA sequencing suggests VPA does not inhibit GSK3b at these concentrations. Knockout of SHROOM3, a well-known NTD-related gene, also caused expansion of the lumen as well as reduced f-actin polarization. The increased lumen sizes were caused by reduced cell apical constriction suggesting that impingement of this process is a shared mechanism for VPA treatment and SHROOM3-KO, two well-known causes of NTDs. Our system allows the rapid identification of NTD-like phenotypes for both compounds and genetic variants and should prove useful for understanding specific NTD mechanisms and predicting drug teratogenicity.

2023-07-19 | GSE232218 | GEO

Shroom3-Fyn interaction determines nephrin phosphorylation and Albuminuria in allografts

Project description:Glomerular RNA-sequencing: Shroom3 knockdown adult mice vs controls

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SHROOM3 Deficiency aggravates Adriamycin-induced nephropathy accompanied by Focal Adhesion disassembly and stress fiber disorganization

Project description:This RNA-sequencing study investigates the role of SHROOM3 in podocyte function and its contribution to renal pathophysiology. Podocytes are highly specialized epithelial cells critical for glomerular filtration barrier integrity. The study explores how SHROOM3 deficiency affects podocyte cytoskeletal architecture and focal adhesion dynamics in the context of Adriamycin-induced nephropathy, a widely used experimental model of podocyte injury and proteinuric kidney disease. We performed transcriptome analysis using RNA-sequencing on human podocyte cell lines, comparing Control (n=4) and SHROOM3 knockdown (KD) podocytes (n=4). Our objective was to identify the molecular mechanisms and signaling pathways through which SHROOM3 regulates podocyte cytoskeletal organization, with particular focus on stress fiber formation and focal adhesion assembly/disassembly. The dataset provides comprehensive gene expression profiles revealing how SHROOM3 deficiency exacerbates podocyte injury, disrupts actin cytoskeleton dynamics, and impairs focal adhesion stability during nephropathy progression.

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Genome-wide association mapping for cardiomyocyte ploidy identifies Shroom3 as responsible for hyperpolyploidy and ventricular dilation

Project description:Cardiomyocyte (CM) polyploidization has been associated with cardiac injury responses, including regeneration and heart failure. However, our understanding of the comprehensive mechanisms governing CM ploidy and its influence on heart physiology has been hindered by a lack of experimental tools. To address this issue and uncover novel genetic regulators, we surveyed CM ploidy across a new genetic resource known as the Hybrid Rat Diversity Panel and find significant variation in ploidy phenotypes across the panel. Using select rat strains with divergent displays of CM ploidy, we found that hyperpolyploidization (≥8N) positively correlates with various physiological parameters namely left ventricular dilation and reduced ejection fraction. Genome-wide association mapping identifies several loci significantly associated with frequency of hyperpolyploid CMs. Investigation of genes harboring damaging protein coding variants identified enrichment of cytoarchitectural genes, of which the ACTIN-binding protein, Shroom3, was found to be strongly and specifically expressed in CMs and harbor 7 damaging protein coding variants. Indeed, CM-specific deletion of Shroom3 increased hyperpolyploidization in adult mice, while also promoting left ventricular dilation and reducing cardiac function. Furthermore, functional characterization of single nucleotide variants resulting in amino acid changes within SHROOM3 confirmed two protein coding variants that disrupted SHROOM3-ACTIN interaction. This study elucidates the genetic determinants of CM ploidy phenotypes and solidifies a relationship between CM ploidy and left ventricular function. Importantly, CM intrinsic expression of at least one gene mapped in this study, Shroom3, is confirmed to regulate CM hyperpolyploidization and cardiac function.

2026-03-25 | GSE307551 | GEO

Genome-wide association mapping for cardiomyocyte ploidy identifies Shroom3 as responsible for hyperpolyploidy and ventricular dilation [bulkRNA-Seq]

Project description:Cardiomyocyte (CM) polyploidy is widely observed across the animal kingdom and various ploidy states are associated with cardiac injury responses, including regeneration and heart failure. However, our understanding of the comprehensive mechanisms governing CM ploidy and its relationship with heart physiology has been hindered by a lack of experimental tools. To address this issue and uncover novel genetic regulators, we surveyed CM ploidy across a new genetic resource known as the Hybrid Rat Diversity Panel and founnd significant variation in ploidy phenotypes across the panel. Using select rat strains with divergent displays of CM ploidy, we found that hyperpolyploidization (≥8N) positively correlates with various physiological parameters namely left ventricular dilation and reduced ejection fraction. Genome-wide association mapping identified several loci significantly associated with frequency of hyperpolyploid CMs. Investigation of genes harboring damaging protein coding variants within these loci identified enrichment of cytoarchitectural genes, of which the ACTIN-binding protein, Shroom3, was found to be strongly and specifically expressed in CMs and harbors 7 damaging protein coding variants. CM-specific deletion of Shroom3 resulted in increased hyperpolyploidization and promoted left ventricular dilation and reduced ejection fraction. Furthermore, functional characterization of single nucleotide variants resulting in amino acid changes within SHROOM3 confirmed two protein coding variants that disrupted SHROOM3-ACTIN interaction and led to altered expression of cell cycle genes. This study elucidates the genetic determinants of CM ploidy phenotypes and solidifies a correlative relationship between CM ploidy and left ventricular function. Importantly, CM intrinsic expression of at least one gene mapped in this study, Shroom3, is confirmed to regulate CM hyperpolyploidization and cardiac function.

2026-03-25 | GSE314057 | GEO

Topological morphogenesis of neuroepithelial organoids.

Project description: Not available

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Epigenome analysis of low-grade neuroepithelial tumors with FGFR2 fusions

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2021-07-27 | GSE172081 | GEO

Gene expression profiling of optic tectum neuroepithelial cells in adult medaka

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