Hedgehog signaling is essential to maintain epithelial identity during larynx and foregut morphogenesis.
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA786580 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17143335.fastq.gz | Fastqsanger.gz | |||
| SRR17143336.fastq.gz | Fastqsanger.gz | |||
| SRR17143337.fastq.gz | Fastqsanger.gz | |||
| SRR17143338.fastq.gz | Fastqsanger.gz |
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Project description:Purpose: This study seeks to determine the role of Hedgehog signaling in larynx development. Methods: To determine how Hedgehog signaling directs larynx epithelial morphogenesis we used genomic approaches to identify a novel set of Hedgehog target genes within the early larynx. To this end, we performed bulk RNA-seq on 3-pooled E10.5 (32-35S) larynx tissues from wild-type (2 replicates) and Shh-/- (2 replicates) embryos. From this experiment we identified 1873 differentially expressed genes (p-value <0.05). Results: Hedgehog is essential for maintaining the identity of foregut-derived epithelial cells within the larynx vocal folds. In the absence of HH signaling these epithelial cells undergo specific transcriptional changes to initiate a partial epithelial-to-mesenchymal transition, migrate out of the epithelial layer and under go cell death. The layer is then replaced by a different population of cells.
2022-11-30 | GSE190281 | GEO
Project description:The larynx, trachea, and esophagus share origin and proximity during embryonic development, with clinical and experimental evidence supporting the existence of neurophysiological, structural, and functional interdependencies before birth. This investigation provides the first comprehensive transcriptional profiling of all three organs during embryonic organogenesis, where differential gene expression gradually assembles the identity and complexity of these proximal organs from a shared origin in the anterior foregut. Through the application of bulk RNA sequencing and gene network analysis of differentially expressed genes (DEGs), both within and across developing embryonic mouse larynx, esophagus, and trachea, we identified co-expressed modules of genes enriched for key biological processes. Organ-specific temporal patterns of gene activity corresponding to gene modules within and across shared tissues during embryonic development (E10.5-E18.5) are described, and the laryngeal transcriptome during vocal fold development and maturation from birth to adult is characterized in the context of laryngeal organogenesis. The findings of this study provide new insights into interrelated gene sets governing organogenesis of this tripartite organ system within the aerodigestive tract, with relevance to multiple families of disorders defined by cardiocraniofacial syndromes.
2022-06-25 | GSE206673 | GEO
Project description:The larynx enables speech while regulating swallowing and respiration. Larynx function hinges on the laryngeal epithelium which originates as part of the anterior foregut and undergoes extensive remodeling to separate from the esophagus and form vocal folds that interface with the adjacent trachea. Here we find that sonic hedgehog (SHH) is essential for epithelial integrity in the mouse larynx as well as the anterior foregut. During larynx-esophageal separation, low Shh expression marks specific domains of actively remodeling epithelium that undergo an epithelial-to-mesenchymal transition (EMT) characterized by the induction of N-Cadherin and movement of cells out of the epithelial layer. Consistent with a role for SHH signaling in regulating this process, Shh mutants undergo an abnormal EMT throughout the anterior foregut and larynx, marked by a cadherin switch, movement out of the epithelial layer and cell death. Unexpectedly, Shh mutant epithelial cells are replaced by a new population of FOXA2-negative cells that likely derive from adjacent pouch tissues and form a rudimentary epithelium. These findings have important implications for interpreting the etiology of HH-dependent birth defects within the foregut. We propose that SHH signaling has a default role in maintaining epithelial identity throughout the anterior foregut and that regionalized reductions in SHH trigger epithelial remodeling.
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Project description:Foregut organogenesis is regulated by inductive interactions between the endoderm and the adjacent mesoderm. We identified genes induced in the foregut progenitors by the adjacent mesoderm. We used microarrays to detail the global programme of early foregut endoderm gene expression resulting from mesoderm induction and identified distinct classes of up-regulated genes during this process. Xenopus foregut endoderm explants cultured from Stages 15 to 23 either intact with mesoderm or as endoderm alone. Total RNA was isolated from the endoderm of these two culture conditions in quadruplicate and were subjected to Affymetrix microarray analysis.
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Project description:The larynx is essential for swallowing, breathing, coughing, and voice production, supported by its unique microbial and immunological environment. Our previous research highlighted the role of resident laryngeal microbiota in shaping local immune responses. With growing interest in the gut-lung axis—the bidirectional communication between gut and respiratory immunity—the potential influence of gut microbiota on laryngeal immunity warrants exploration. We hypothesized that a gut-larynx axis may exist, where both resident laryngeal and gut microbiota contribute to immune modulation in the larynx. To investigate this, we treated conventionally raised, wild-type C57BL/6J mice with an oral antibiotic regimen known to disrupt gut microbiota, comparing them to untreated controls. Following treatment, the gut microbiota was significantly disrupted, while the laryngeal microbiota remained largely unchanged. However, antibiotic-treated mice exhibited marked changes in epithelial and immune cell proportions, as well as fibroblasts. Differential gene expression across cell types highlighted pathways related to epithelial barrier integrity, immune signaling, and bacterial response. Additionally, gut dysbiosis affected gene regulatory networks, with the activity of regulons Etv4(+), Irf3(+), Hltf(+), Mga(+), and Nfil3(+) showing significant changes. Notably, cell-cell communication was also altered, especially in immune-epithelial interactions, with integrin-mediated signaling emerging as a key ligand-receptor pathway in these intercellular communications. These findings suggest that gut and laryngeal microbiota may work synergistically to modulate immune responses in the larynx, underscoring the importance of considering gut-larynx interactions in studies of respiratory immunity.
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Project description:Foregut organogenesis is regulated by inductive interactions between the endoderm and the adjacent mesoderm. We identified genes induced in the foregut progenitors by the adjacent mesoderm. We used microarrays to detail the global programme of early foregut endoderm gene expression resulting from mesoderm induction and identified distinct classes of up-regulated genes during this process.
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Project description:Adult Drosophila foregut contains a diverse set of tissue and cell types. We applied single cell RNA sequencing (scRNA-seq) and bulk RNA sequencing (bulk RNA-seq) to delineate the cellular composition and molecular profile of the foregut and its associated physiological functions.
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Project description:Postnatal tissue quiescence is generally thought to be a default state in the absence of a proliferative stimulus such as injury. We now demonstrate that in the lung, quiescence in the adult is an actively maintained state and is regulated by paracrine hedgehog signaling. Epithelial-specific deletion of Sonic Hedgehog during normal homeostasis results in a proliferative expansion of the adjacent lung mesenchyme. Injury to the lung epithelium results in decreased hedgehog activation, accompanied by proliferative expansion of the adjacent mesenchyme. Moreover, reconstitution of Hedgehog signaling during epithelial injury attenuated the proliferative expansion of the adjacent mesenchyme. Hedgehog signaling maintains lung quiescence by attenuating PDGF signaling through blocking post-translational processing of PDGF receptor α/β into the mature isoforms. These results indicate that in postnatal tissues, epithelial cells can actively maintain mesenchymal quiescence via paracrine hedgehog activation, and that imbalances in this pathway could lead to aberrant mesenchymal expansion and postnatal disease. Fibroblasts were isolated from mouse lungs and grown in culture in triplicate wells. Samples were treated with vehicle or purmorphamine 5um for 24 hours and RNA was isolated for microarray.
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