Drosophila single-cell expression data of enteroendocrine cell lineage-traced guts, and guts under control and Xrp1 overexpression conditions in enteroendocrine cells.
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ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE301623 | GEO | 2025/07/05
REPOSITORIES: GEO
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Project description:Drosophila single-cell expression data of enteroendocrine cell lineage-traced guts, and guts under control and Xrp1 overexpression conditions in enteroendocrine cells.
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Project description:Differentiated cells exhibit cell plasticity, where they dedifferentiate to stem cells or trans-differentiate into cells of another lineage, when necessary. We studied the cell plasticity of secretory enternendocrine cells (EEs) in the fruit fly Drosophila melanogaster. We resolved single-cell transcriptomics of EEs and cells derived from EEs. Our scRNA-seq data of EE lineages have characterized intermediate cell types derived from EEs. We also specifically focused on a gene called Xrp1 and examined potential changes of all epithelial cell types by EE-specific Xrp1 overexpression (O/E). Our scRNA-seq data of Xrp1 O/E EEs have provided evidence on changes in gene expression profiles of each cell type by Xrp1 O/E in EEs.
2025-07-07 | GSE295684 | GEO
Project description:Whereas complete loss of Rp function is generally lethal, most heterozygous Rp mutants grow more slowly and are subject to competitive loss from mosaics tissues that also contain wild type cells. The rpS12 gene has a special role in the cell competition of other Ribosomal Protein (Rp) mutant cells in Drosophila. Elimination by cell competition is promoted by higher RpS12 levels and prevented by a specific rpS12 mis-sense mutation, identifying RpS12 as a key effector of cell competition due to mutations in other Rp genes. Here we show that RpS12 is also required for other aspects of Rp mutant phenotypes, including hundreds of gene expression changes that occur in 'Minute' Rp heterozygous wing imaginal discs, overall translation rate, and the overall rate of organismal development, all through the bZip protein Xrp1 that is one of the RpS12-regulated genes. Our findings outline the regulatory response to mutations affecting essential Rp genes that controls overall translation, growth, and cell competition, and which may contribute to cancer and other diseases.
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Project description:Single-cell level gene expression profiles of enteroendocrine cell lineages, control guts and guts with Xrp1 overexpressed in EEs
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Project description:Intestinal stem cells in the adult Drosophila midgut are regulated by growth factors produced from the surrounding niche cells including enterocytes and visceral muscle. The role of the other major cell type, the secretory enteroendocrine cells, in regulating intestinal stem cells remains unclear. We show here that newly eclosed scute loss-of-function mutant flies are completely devoid of enteroendocrine cells. These enteroendocrine cell-less flies have normal ingestion and fecundity but shorter lifespan. Moreover, in these newly eclosed mutant flies, the diet-stimulated midgut growth that depends on the insulin-like peptide 3 expression in the surrounding muscle is defective. The depletion of Tachykinin-producing enteroendocrine cells or knockdown of Tachykinin leads to a similar although less severe phenotype. These results establish that enteroendocrine cells serve as an important link between diet and visceral muscle expression of an insulin-like growth factor to stimulate intestinal stem cell proliferation and tissue growth.
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Project description:Transcription factor Neurod1 is required for enteroendocrine progenitor differentiation and maturation. Several earlier studies indicated that ectopic expression of Neurod1 converted non- neuronal cells into neurons. However, the functional consequence of ectopic Neurod1 expression has not been examined in the GI tract, and it is not known whether Neurod1 can similarly switch cell fates in the intestine. We generated a mouse line that would enable us to conditionally express Neurod1 in intestinal epithelial cells at different stages of differentiation. Forced expression of Neurod1 throughout intestinal epithelium increased the number of EECs as well as the expression of EE specific transcription factors and hormones. Furthermore, we observed a substantial reduction of Paneth cell marker expression, although the expressions of enterocyte-, tuft- and goblet-cell specific markers are largely not affected. Our earlier study indicated that Neurog3+ progenitor cells give rise to not only EECs but also Goblet and Paneth cells. Here we show that the conditional expression of Neurod1 restricts Neurog3+ progenitors to adopt Paneth cell fate, and promotes more pronounced EE cell differentiation, while such effects are not seen in more differentiated Neurod1+ cells. Together, our data suggest that forced expression of Neurod1 programs intestinal epithelial cells more towards an EE cell fate at the expense of the Paneth cell lineage and the effect ceases as cells mature to EE cells.
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Project description:Several cell populations have been reported to possess intestinal stem cell (ISC) activity during homeostasis and injury-induced regeneration. Here, we explored inter-relationships between putative mouse ISC populations by comparative RNA-sequencing (RNA-seq). The transcriptomes of multiple cycling ISC populations closely resembled Lgr5+ ISCs, the most well-defined ISC pool, but Bmi1-GFP+ cells were distinct and enriched for enteroendocrine (EE) markers, including Prox1. Prox1-GFP+ cells exhibited sustained clonogenic growth in vitro, and lineage-tracing of Prox1+ cells revealed long-lived clones during homeostasis and after radiation-induced injury in vivo. Single-cell mRNA-seq revealed two subsets of Prox1-GFP+ cells, one of which resembled mature EE cells while the other displayed low-level EE gene expression but co-expressed tuft cell markers, Lgr5 and Ascl2, reminiscent of label-retaining secretory progenitors. Our data suggest that the EE lineage, including mature EE cells, comprises a reservoir of homeostatic and injury-inducible ISCs, extending our understanding of cellular plasticity and stemness.
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Project description:Simultaneous profiling of single-cell gene expression and lineage history holds enormous potential for studying cellular decision-making. Recent computational approaches combine both modalities into cellular trajectories; however, they cannot make use of all available lineage information in destructive time-series experiments. Here, we present moslin, a Gromov-Wasserstein-based model to couple cellular profiles across time points based on lineage and gene expression information. We validate our approach in simulations and demonstrate on Caenorhabditis elegans embryonic development how moslin predicts fate probabilities and putative decision driver genes. Finally, we use moslin to delineate lineage relationships among transiently activated fibroblast states during zebrafish heart regeneration.
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Project description:Testing is recommended for all close contacts of confirmed COVID-19 patients. However, existing pooled testing methods are oblivious to the circumstances of contagion provided by contact tracing. Here, we build upon a well-known semi-adaptive pooled testing method, Dorfman's method with imperfect tests, and derive a simple pooled testing method based on dynamic programming that is specifically designed to use information provided by contact tracing. Experiments using a variety of reproduction numbers and dispersion levels, including those estimated in the context of the COVID-19 pandemic, show that the pools found using our method result in a significantly lower number of tests than those found using Dorfman's method. Our method provides the greatest competitive advantage when the number of contacts of an infected individual is small, or the distribution of secondary infections is highly overdispersed. Moreover, it maintains this competitive advantage under imperfect contact tracing and significant levels of dilution.
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Project description:Enteroendocrine cells (EEs) represent a heterogeneous cell population in intestine and exert endocrine functions by secreting a diverse array of neuropeptides. Although many transcription factors (TFs) required for specification of EEs have been identified in both mammals and Drosophila, it is not understood how these TFs work together to generate this considerable subtype diversity. Here we show that EE diversity in adult Drosophila is generated via an "additive hierarchical TF cascade". Specifically, a combination of a master TF, a secondary-level TF and a tertiary-level TF constitute a "TF code" for generating EE diversity. We also discover a high degree of post-specification plasticity of EEs, as changes in the code-including as few as one distinct TF-allow efficient switching of subtype identities. Our study thus reveals a hierarchically-organized TF code that underlies EE diversity and plasticity in Drosophila, which can guide investigations of EEs in mammals and inform their application in medicine.
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