Arabidopsis thaliana
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA257644 | ENA |
REPOSITORIES: ENA
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Project description:Extracellular signaling and nutrient availability are major factors for cell fate decision. Responds to extracellular information requires metabolic alterations and differential gene expression. However, how cells integrate extracellular signals (e.g. hormones) and cellular metabolic status to coordinate transcriptional outcome is poorly understood. We hypothesized that fluctuations in nuclear nicotinamide adenine dinucleotide (NAD+) levels act as a signal to integrate cellular glucose metabolism and transcription program during adipocyte differentiation. To test this hypothesis, we performed RNA-seq on control, Nmnat1 and Parp1 knockdown 3T3-L1 cells during various time point of differentiation.
2018-03-17 | GSE96764 | GEO
Project description:Histones, major carriers of epigenetic information, play critical roles in regulating gene expression patterns and cell fate decisions. While asymmetric histone inheritance has been shown to regulate distinct cell fates in Drosophila adult stem cells, its relevance in mammals remains unclear. In this study, we investigated cell division modes and histone inheritance patterns in horizontal basal cells (HBCs) of the mouse olfactory epithelium following injury. We found that approximately 40% of telophase HBCs show asymmetric division, with a corresponding asymmetric segregation of histone H4. In primary cultured HBCs, we observed asymmetric cell division accompanied by asymmetric distribution of histones, including H4, H3, and H3.3, but not H2A-H2B. Asymmetric histone segregation leads to asymmetric association of a key ‘stemness’ transcription factor p63 and asynchronous transcription re-initiation during mitotic exit. Single-cell RNA sequencing of paired daughter cells further revealed asymmetric cell fate priming in cultured HBCs. Disruption of asymmetric cell division abolished asymmetric transcription re-initiation, asymmetric histone inheritance in culture HBCs and further caused regeneration defects in OE. These findings reveal the conservation of asymmetric histone inheritance in mammalian adult stem cells and highlight its biological significance in tissue regeneration.
2025-03-26 | GSE286046 | GEO
Project description:The development of a complex organ requires the proper differentiation and production of appropriate numbers of each of its constituent cell types, as well as their correct positioning within the organ. During Drosophila cardiogenesis, all three of these processes are controlled by jumeau (jumu) and Checkpoint suppressor homologue (CHES-1-like), two genes encoding forkhead transcription factors that were discovered utilizing an integrated genetic, genomic and computational strategy which identified 70 novel genes expressed in the developing Drosophila heart. Both jumu and CHES-1-like are required during asymmetric cell division for the derivation of two distinct cardiac cell types from their mutual precursor, and in symmetric cell division to produce yet a third type of heart cell. jumu and CHES-1-like control the division of cardiac progenitors by regulating the activity of Polo, a kinase involved in multiple steps of mitosis. This pathway demonstrates how transcription factors integrate diverse developmental processes during organogenesis. GFP-positive cells were profiled from Stage 11-12 Drosophila embryos of the following two genotypes: twi-GAL4 UAS-2EGFP/UAS-jumu and twi-GAL4 UAS-2EGFP
2012-01-30 | E-GEOD-34946 | biostudies-arrayexpress
Project description:Satellite cells are adult muscle stem cells responsible for muscle regeneration after acute or chronic injuries. The balance between stem cell self-renewal and differentiation impacts the kinetics and efficiency of skeletal muscle regeneration. This study elucidated the function of Islr in satellite cell asymmetric division. Satellite cell specific deletion of Islr compromises muscle regeneration in adult mice by impairing the satellite cell pool. Islr is pivotal for satellite cell proliferation and its deletion promotes asymmetric cell fate segregation of satellite cells. A mechanistic search revealed that Islr interacts and stabilizes the Sparc protein, which activates p-ERK1/2 signaling required for asymmetric division. In combination, the findings have identified Islr as a key regulator of satellite cell asymmetric division through the Sparc/p-ERK1/2 signaling pathway, which provides a new insight into satellite cell biology and open avenues for the treatment of myopathy.
2023-08-16 | GSE210951 | GEO
Project description:Cellular metabolism is emerging as a potent regulator of cell fate, raising the possibility that the recently discovered metabolic heterogeneity between newly synthesized and chronologically old organelles may impact stem cell fate in mammalian tissues. The small intestine is maintained by actively cycling intestinal stem cells (ISCs) that give rise to metabolically distinct progeny, including their Paneth cell niche. Here, we find that asymmetric cell division generates a subset of ISCs enriched for old mitochondria (ISCmito-O). Although ISCmito-O lack characteristics of reserve stem cells, they form organoids niche-independently, owing to their ability to recreate the Paneth cell niche. Mechanistically, mitochondria in ISCmito-O generate more alpha-ketoglutarate (aKG), driving ten-eleven translocation (Tet) methylcytosine dioxygenase-mediated epigenetic changes that are associated with differentiation towards the Paneth cell fate. aKG supplementation in vivo promotes Paneth cell turnover leading to niche renewal, which promotes recovery from chemotherapy-induced damage in aged animals. Our results reveal a subpopulation of intestinal stem cells whose old mitochondria metabolically regulate cell fate, and provide proof-of-principle for metabolically promoted replacement of specific aged cell types in vivo.
2025-04-24 | MTBLS12349 | MetaboLights
Project description:During cerebral cortex development, neural stem cells (NSCs) require precise spatiotemporal signals to acquire the correct cell identity at the exact moment. Even though epigenetic regulation plays a central role in cell fate decisions, the exact mechanisms remain elusive. Thus, we focus our research on the H3K79 methyltransferase DOT1L, a key player in cell fate decisions. Our group has shown that DOT1L prevents NSC premature differentiation by increasing expression of genes that regulate asymmetric cell division (Franz et al. 2019). Using cell-lineage tracing and pharmacological inhibition, we confirmed that when DOT1L is inhibited apical progenitors (APs) switch to symmetric neurogenic divisions in detriment of asymmetric self-renewal (Appiah et al. 2023). We now analyse conditional knockout (cKO) and control (WT) mice for DOT1L using Emx1-Cre line during cortical mid-neurogenesis (E14.5) using single cell RNA-seq to understand how the transcriptome changes.
2025-07-30 | GSE291845 | GEO
Project description:Metabolic characteristics of adult stem cells are distinct from their differentiated progeny, and cellular metabolism is emerging as a potential driver of cell fate conversions. However, how metabolism influences fate determination remains unclear. Here, we identified inherited metabolism imposed by functionally distinct mitochondrial age-classes as a fate determinant in asymmetric division of epithelial stem-like cells. While chronologically old mitochondria support oxidative respiration, new organelles are immature and metabolically less active. Upon cell division, selectively segregated mitochondrial age-classes elicit a metabolic bias in progeny cells, with old mitochondria imposing oxidative energy metabolism inducing differentiation. High pentose phosphate pathway flux, promoting redox maintenance, is favoured in cells receiving newly synthesised mitochondria, and is required to maintain stemness during early fate determination after division. Our results demonstrate that fate decisions are susceptible to intrinsic metabolic bias imposed by selectively inherited mitochondria.
2021-12-20 | PXD010667 | Pride
Project description:How tissues generate asymmetric growth from spatially and temporally restricted signals remains a fundamental challenge in developmental biology. We show that transient cell states encode positional information that instructs asymmetric growth in plants. Using spatial single-cell transcriptomics and multi-omics, we uncover a surprisingly complex landscape of transient cell states in the apical hook, including a previously unrecognized population in the apical hypocotyl region that integrates developmental and hormonal cues and bifurcates into opposing growth trajectories. Gene regulatory network analysis and functional perturbation establish GATA TRANSCRIPTION FACTOR 2 (GATA2) as a central regulator that promotes cell elongation through gibberellin signaling. These results reveal that diverse, spatially localized transient cell states function as regulatory hubs that convert positional information into divergent growth programs, providing a unifying framework for how dynamic cellular states shape organ morphology.
2026-08-10 | GSE327709 | GEO
Project description:How tissues generate asymmetric growth from spatially and temporally restricted signals remains a fundamental challenge in developmental biology. We show that transient cell states encode positional information that instructs asymmetric growth in plants. Using spatial single-cell transcriptomics and multi-omics, we uncover a surprisingly complex landscape of transient cell states in the apical hook, including a previously unrecognized population in the apical hypocotyl region that integrates developmental and hormonal cues and bifurcates into opposing growth trajectories. Gene regulatory network analysis and functional perturbation establish GATA TRANSCRIPTION FACTOR 2 (GATA2) as a central regulator that promotes cell elongation through gibberellin signaling. These results reveal that diverse, spatially localized transient cell states function as regulatory hubs that convert positional information into divergent growth programs, providing a unifying framework for how dynamic cellular states shape organ morphology.
2026-08-10 | GSE327163 | GEO
Project description:How tissues generate asymmetric growth from spatially and temporally restricted signals remains a fundamental challenge in developmental biology. We show that transient cell states encode positional information that instructs asymmetric growth in plants. Using spatial single-cell transcriptomics and multi-omics, we uncover a surprisingly complex landscape of transient cell states in the apical hook, including a previously unrecognized population in the apical hypocotyl region that integrates developmental and hormonal cues and bifurcates into opposing growth trajectories. Gene regulatory network analysis and functional perturbation establish GATA TRANSCRIPTION FACTOR 2 (GATA2) as a central regulator that promotes cell elongation through gibberellin signaling. These results reveal that diverse, spatially localized transient cell states function as regulatory hubs that convert positional information into divergent growth programs, providing a unifying framework for how dynamic cellular states shape organ morphology.
2026-08-10 | GSE326975 | GEO