A single-cell atlas of Drosophila trachea reveals glycosylation-mediated Notch signaling in cell fate specification
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ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE240777 | GEO | 2024/02/18
REPOSITORIES: GEO
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Project description:A single-cell atlas of Drosophila trachea reveals glycosylation-mediated Notch signaling in cell fate specification
| PRJNA1005234 | ENA
Project description:Abstract: The Drosophila trachea is a branched tubular epithelia that transports oxygen and other gases. trachealess (trh), which encodes a bHLH-PAS transcription factor, is among the first genes to be expressed in the cells that will form the trachea. In the absence of trh, tracheal cells fail to invaginate to form tubes and remain on the embryo surface. Expression of many tracheal-specific genes depends on trh, but all of the known targets have relatively minor phenotypes compared to loss of trh, suggesting that there are additional targets. To identify uncharacterized transcriptional targets of Trh and to further understand the role of Trh in embryonic tracheal formation, we performed an in situ hybridization screen using a library of ~100 tracheal-expressed genes identified by the Berkeley Drosophila Genome Project (BDGP). Surprisingly, expression of every tracheal gene we tested was dependent on Trh, suggesting a major role for Trh in activation and maintenance of tracheal gene expression. A re-examination of the interdependence of the known early-expressed transcription factors, including trh, ventral veinless (vvl) and knirps/knirps-related (kni/knrl), suggests a new model for how gene expression is controlled in the trachea, with trh regulating expression of vvl and kni, but not vice versa. A pilot screen for the targets of Vvl and Kni/Knrl revealed that Vvl and Kni have only minor roles compared to Trh. Finally, genome-wide microarray experiments identified additional Trh targets and revealed that a of biological processes are affected by the loss of trh. Goals: The goals of the microarray experiments were to identify additional targets of the Trh transcription factor to learn the range of genes regulated by this transcription factor during embryogenesis. Our in situ screen revealed that Trh is required for all tested tracheal genes. Our new data now shows that Trh affects a range of biological processes. RNA was isolated from stage 11-16 wild type Drosophila embryos and compared to RNA from trh null mutant embryos of the same age; all samples were hybridized to the Drosophila Genome 2.0 Affymetrix array. Three individual replicates were obtained for each sample.
2011-12-21 | E-GEOD-28780 | biostudies-arrayexpress
Project description:Abstract: The Drosophila trachea is a branched tubular epithelia that transports oxygen and other gases. trachealess (trh), which encodes a bHLH-PAS transcription factor, is among the first genes to be expressed in the cells that will form the trachea. In the absence of trh, tracheal cells fail to invaginate to form tubes and remain on the embryo surface. Expression of many tracheal-specific genes depends on trh, but all of the known targets have relatively minor phenotypes compared to loss of trh, suggesting that there are additional targets. To identify uncharacterized transcriptional targets of Trh and to further understand the role of Trh in embryonic tracheal formation, we performed an in situ hybridization screen using a library of ~100 tracheal-expressed genes identified by the Berkeley Drosophila Genome Project (BDGP). Surprisingly, expression of every tracheal gene we tested was dependent on Trh, suggesting a major role for Trh in activation and maintenance of tracheal gene expression. A re-examination of the interdependence of the known early-expressed transcription factors, including trh, ventral veinless (vvl) and knirps/knirps-related (kni/knrl), suggests a new model for how gene expression is controlled in the trachea, with trh regulating expression of vvl and kni, but not vice versa. A pilot screen for the targets of Vvl and Kni/Knrl revealed that Vvl and Kni have only minor roles compared to Trh. Finally, genome-wide microarray experiments identified additional Trh targets and revealed that a of biological processes are affected by the loss of trh. Goals: The goals of the microarray experiments were to identify additional targets of the Trh transcription factor to learn the range of genes regulated by this transcription factor during embryogenesis. Our in situ screen revealed that Trh is required for all tested tracheal genes. Our new data now shows that Trh affects a range of biological processes.
2011-12-21 | GSE28780 | GEO
Project description:We performed a single-cell analysis of the larval tracheal system of Drosophila melanogaster and identified a total of 17 distinct cell populations that are part of or closely associated with the trachea.
2023-10-31 | GSE240638 | GEO
Project description:Ion channels play critical roles in the physiology and function of the nervous system and contractile tissue; however, their role in non-contractile tissue and embryonic development has yet to be understood. Tracheobronchomalacia (TBM) and complete tracheal rings (CTR) are disorders affecting the muscle and cartilage of the trachea and bronchi, whose etiology remains poorly understood. We demonstrated that trachealis muscle organization and polarity are disrupted after epithelial ablation of Wls, a cargo receptor critical for the Wnt signaling pathway, in developing trachea. The phenotype resembles the anomalous trachealis muscle observed after deletion of ion channel encoding genes in developing mouse trachea. We sought to investigate whether and how the deletion ofWlsaffects ion channels during tracheal development. We hypothesize that Wnt signaling influences the expression of ion channels to promote trachealis muscle cell assembly and patterning. Deleting Wls in developing trachea causes differential regulation of genes mediating actin binding, cytoskeleton organization, and potassium ion channel activity. Wnt signaling regulated expression of Kcnj13, Kcnd3, Kcnj8, and Abcc9 as demonstrated by in vitro studies and in vivo analysis in Wnt5a and b-catenin deficient tracheas. Pharmacological inhibition of potassium ion channels and Wnt signaling impaired contractility of developing trachealis smooth muscle and formation of cartilaginous mesenchymal condensation. Thus, in mice, epithelial-induced Wnt/b-catenin signaling mediates trachealis muscle and cartilage development via modulation of ion channel expression, promoting trachealis muscle architecture, contractility, and cartilaginous extracellular matrix. In turn, ion channel activity may influence tracheal morphogenesis underlying TBM and CTR.
2023-11-06 | GSE241175 | GEO
Project description:Adult stem cells are essential for maintaining tissue homeostasis. We employ Drosophila tracheal progenitors to understand the mechanism controlling the polarity of stem cell migration. Here, we show that polarity of tracheal progenitors depends on the function of fat body. Cytokine, Upd2, produced by fat body, signals to tracheal progenitors and activation JAK/STAT signal transduction. Perturbation of Upd2 production or loss-of-function of JAK/STAT signaling in the trachea cause aberrant bidirectional migration of tracheal progenitors. JAK/STAT signaling promotes the expression of a series of genes involved in planar cell polarity, which generates asymmetric localization of Fat and Pod1. Furthermore, the transport of Upd2 requires Rab5-, Rab7-mediated endocytic sorting and Lbm-dependent vesicle trafficking, where vesicular Upd2 functionally interacts with Rabs, Tetraspanin and Grasp65. These results reveal an inter-organ communication in which cytokines from fat body direct the polarity of ectodermal origin tracheal progenitors and suggest that Upd2-dependent JAK/STAT signaling regulates anterior-posterior polarity of tracheal progenitor movement.
2024-10-28 | GSE256177 | GEO
Project description:To further identify the transcriptional changes underlying congenital tracheal malformation in a1H knockout mice, the differential gene expression panel was examined by Affymetrix microarray. To investigate the roles of a1H-regulated genes in tracheal development, we characterize the unique transcriptional changes of early trachea in kockout mice, and compare the expression profiles of knock out trachea with those of wild type trachea. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up or down-regulated genes during this process. Mouse embryos trachea were collected at embryo day 16 (E16) for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain homozygous mouse embryos trachea in order to compare with gene expression profile of wild type mouse tracheal.
2014-02-14 | E-GEOD-27305 | biostudies-arrayexpress
Project description:Sivakumar2011 - Hedgehog Signaling Pathway
This is the current model for the Hedgehog signaling pathway. The best data for mechanism of signaling has been worked out in Drosophila, so this model is based largely on Drosophila data. Hedgehog target genes vary from tissue to tissue, so the identities of individual target genes have not been listed. The main difference between the Drosophila and mammalian Hedgehog signaling pathways is the fact that there are three mammalian homologs of Cubitus interruptus, Gli1 Gli2 and Gli3. Some or all of the mammalian homologs may be proteolytically processed, but the data are controversial. There are two mammalian Ptc genes and three mammalian Hedgehog genes as well. The pathway for Sonic Hedgehog appears to be most similar to the Drosophila hedgehog pathway.
References:
Hedgehog signaling in animal development: paradigms and principles.
Sonic hedgehog in the nervous system: functions, modifications and mechanisms.
Hedgehog signal transduction: recent findings.
Hedgehog signaling: Costal-2 bridges the transduction gap.
This model is described in the article:
A systems biology approach to model neural stem cell regulation by notch, shh, wnt, and EGF signaling pathways.
Sivakumar KC, Dhanesh SB, Shobana S, James J, Mundayoor S.
Omics: a Journal of Integrative Biology. 2011; 15(10):729-737
Abstract:
The Notch, Sonic Hedgehog (Shh), Wnt, and EGF pathways have long been known to influence cell fate specification in the developing nervous system. Here we attempted to evaluate the contemporary knowledge about neural stem cell differentiation promoted by various drug-based regulations through a systems biology approach. Our model showed the phenomenon of DAPT-mediated antagonism of Enhancer of split [E(spl)] genes and enhancement of Shh target genes by a SAG agonist that were effectively demonstrated computationally and were consistent with experimental studies. However, in the case of model simulation of Wnt and EGF pathways, the model network did not supply any concurrent results with experimental data despite the fact that drugs were added at the appropriate positions. This paves insight into the potential of crosstalks between pathways considered in our study. Therefore, we manually developed a map of signaling crosstalk, which included the species connected by representatives from Notch, Shh, Wnt, and EGF pathways and highlighted the regulation of a single target gene, Hes-1, based on drug-induced simulations. These simulations provided results that matched with experimental studies. Therefore, these signaling crosstalk models complement as a tool toward the discovery of novel regulatory processes involved in neural stem cell maintenance, proliferation, and differentiation during mammalian central nervous system development. To our knowledge, this is the first report of a simple crosstalk map that highlights the differential regulation of neural stem cell differentiation and underscores the flow of positive and negative regulatory signals modulated by drugs.
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2024-09-02 | BIOMD0000000395 | BioModels
Project description:To further identify the transcriptional changes underlying congenital tracheal malformation in a1H knockout mice, the differential gene expression panel was examined by Affymetrix microarray. To investigate the roles of a1H-regulated genes in tracheal development, we characterize the unique transcriptional changes of early trachea in kockout mice, and compare the expression profiles of knock out trachea with those of wild type trachea. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up or down-regulated genes during this process.
2014-02-14 | GSE27305 | GEO
Project description:Dr. Stanley's laboratory is interested in determining how O-fucose glycans function in Notch receptor signaling and in modulating the interactions of Notch receptors with their ligands. We have generated mice carrying a point mutation in the ligand binding domain of Notch1 that reduces Notch ligand binding to mutant T cells. We wish to identify Notch target genes including glycosylation genes with altered expression in DP thymic T cells from mutant and control mice.
2011-04-29 | GSE28936 | GEO