Ontology highlight
ABSTRACT:
PROVIDER: PRJNA686137 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13297222_1.fastq.gz | Fastqsanger.gz | |||
| SRR13297222_2.fastq.gz | Fastqsanger.gz | |||
| SRR13297223_1.fastq.gz | Fastqsanger.gz | |||
| SRR13297223_2.fastq.gz | Fastqsanger.gz | |||
| SRR13297224_1.fastq.gz | Fastqsanger.gz |
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Project description:Single-minded 2 is required for left-right asymmetric stomach morphogenesis
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Project description:Structural birth defects are the leading cause of infant mortality in the United States. Many of these defects are associated with abnormal anatomical left-right asymmetry. Despite the importance of orienting organs along the left-right (L-R) axis during development, very little is known about the molecular events that control this process. To elucidate the genetic mechanisms that shape the L-R asymmetry of individual organs, we sought to identify genes that are expressed in L-R asymmetric patterns during organ development. To accomplish this goal, we took advantage of the exceptionally large Budgett’s frog (Lepidobatrachus laevis) embryo to profile gene expression by RNA-seq in the left versus right halves of the developing stomach. Using this data, we have constructed a de novo Lepidobatrachus transcriptome and identified ~26,000 unique transcripts with human homology based on reciprocal BLAST analyses. Over 300 transcripts were L-R asymmetrically expressed within the stomach. Among these candidates are some of the few genes already known to play a role in L-R asymmetric development, validating our strategy for L-R gene discovery.
2023-05-26 | GSE99817 | GEO
Project description:The secreted factor Nodal has been shown to be a major left determinant. Although it is associated with severe congenital heart defects, its role in heart morphogenesis has remained poorly understood. Here, we report that Nodal is transiently active in precursors of the mouse heart tube poles, before the morphological changes of heart looping. In conditional mutants, we show that Nodal is not required to initiate asymmetric morphogenesis. We provide evidence of a heart-specific random generator of asymmetry that is independent of Nodal. Using 3D quantifications and simulations, we demonstrate that Nodal functions as a bias of this mechanism: it is required to amplify and coordinate opposed left-right asymmetries at the heart tube poles, thus generating a robust helical shape. We identify downstream effectors of Nodal signalling, regulating asymmetries in cell proliferation, cell differentiation and extra-cellular matrix composition. Our work provides novel insight into how Nodal regulates asymmetric organogenesis.
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Project description:The vagus nerves are important carriers of sensory information from the viscera to the central nervous system. Emerging evidence suggests that sensory signaling through the right, but not the left, vagus nerve evokes striatal dopamine release and reinforces appetitive behaviors. However, the extent to which differential gene expression within vagal sensory neurons contributes to this asymmetric reward-related signaling remains unknown. Here, we use single-cell RNA sequencing to identify genes that are differentially expressed between the left and right nodose ganglia (NG) to identify candidate genes likely to contribute to vagus-mediated reward signaling. We find that a group of neurons expressing Chrna3 (nicotinic acetylcholine receptor subunit 3) and Cckar (cholecystokinin A receptor) is preferentially expressed in the right NG of both rats and mice. This result suggests that differential expression of gut-innervating nutrient sensors in NG neurons may contribute to asymmetric encoding of interoceptive rewards by the vagus nerves.
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Project description:The effect of MAN1A2 on biliary morphogenesis, left-right patterning, and ciliogenesis was evaluated with knockdown in zebrafish and subsequent RNAseq experiment/analysis.
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Project description:Diverse functions of the homeodomain transcription factor BARX1 include Wnt-dependent, non-cell autonomous specification of the stomach epithelium, tracheo-bronchial septation, and Wnt-independent expansion of the spleen primordium. Tight spatio-temporal regulation of Barx1 levels in the mesentery and stomach mesenchyme suggests additional roles. To determine these functions, we forced constitutive BARX1 expression in the Bapx1 expression domain, which includes the mesentery and intestinal mesenchyme, and also examined Barx1-/- embryos in further detail. Transgenic embryos invariably showed intestinal truncation and malrotation, in part reflecting abnormal left-right patterning. Ectopic BARX1 expression did not affect intestinal epithelium, but intestinal smooth muscle developed with features typical of the stomach wall. BARX1, which is normally restricted to the developing stomach, drives robust smooth muscle expansion in this organ by promoting proliferation of myogenic progenitors at the expense of other sub-epithelial cells. Undifferentiated embryonic stomach and intestinal mesenchyme showed modest differences in mRNA expression and BARX1 was sufficient to induce much of the stomach profile in intestinal cells. However, limited binding at cis-regulatory sites implies that BARX1 may act principally through other transcription factors. Genes expressed ectopically in BARX1+ intestinal mesenchyme and reduced in Barx1-/- stomach mesenchyme include Isl1, Pitx1, Six2 and Pitx2, transcription factors known to control left-right patterning and influence smooth muscle development. The sum of evidence suggests that potent BARX1 functions in intestinal rotation and stomach myogenesis occur through this small group of intermediary transcription factors.
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Project description:Diverse functions of the homeodomain transcription factor BARX1 include Wnt-dependent, non-cell autonomous specification of the stomach epithelium, tracheo-bronchial septation, and Wnt-independent expansion of the spleen primordium. Tight spatio-temporal regulation of Barx1 levels in the mesentery and stomach mesenchyme suggests additional roles. To determine these functions, we forced constitutive BARX1 expression in the Bapx1 expression domain, which includes the mesentery and intestinal mesenchyme, and also examined Barx1-/- embryos in further detail. Transgenic embryos invariably showed intestinal truncation and malrotation, in part reflecting abnormal left-right patterning. Ectopic BARX1 expression did not affect intestinal epithelium, but intestinal smooth muscle developed with features typical of the stomach wall. BARX1, which is normally restricted to the developing stomach, drives robust smooth muscle expansion in this organ by promoting proliferation of myogenic progenitors at the expense of other sub-epithelial cells. Undifferentiated embryonic stomach and intestinal mesenchyme showed modest differences in mRNA expression and BARX1 was sufficient to induce much of the stomach profile in intestinal cells. However, limited binding at cis-regulatory sites implies that BARX1 may act principally through other transcription factors. Genes expressed ectopically in BARX1+ intestinal mesenchyme and reduced in Barx1-/- stomach mesenchyme include Isl1, Pitx1, Six2 and Pitx2, transcription factors known to control left-right patterning and influence smooth muscle development. The sum of evidence suggests that potent BARX1 functions in intestinal rotation and stomach myogenesis occur through this small group of intermediary transcription factors. To investigate how Barx1 regulates gut smooth muscle development in a cell-autonomous manner, we used Affymetrix arrays to profile genes enriched in wild-type stomach and BARX1-overexpressing intestinal mesenchyme, compared to wild-type intestinal mesenchyme.
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Project description:14 days after a single subcutaneous monocrotaline (MCT) injection we isolated the left and right ventricles from wistar rats. Factor1: Comparison between control (CON), compensated hypertrophy (HYP), and decompensated hypertrophy (CHF). Factor2: Comparison between left ventricle (LV) and right ventricle (RV). Keywords: dose response
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Project description:The role of CRTH2 (chemoattractant receptor) in a murine allergic contact inflammation model of human Atopic Dermatitis was investigated.This an acute model of atopic dermatitis in which a CRTH2 antagonist (compound A) and a positive control drug (dexamethasone, Dex) were evaluated. The experimental protocol was as follows:the mice first had their stomach area shaved, and either FITC (Fluorescein isothiocyanate) or the vehicle FITC is dissolved in (acetone:DBPTH) is applied to the skin on day 1 and day 2. The mouse generated an immune response to FITC and made specific antibodies. Six days later, the mouse was challenged, which consisted of putting FITC on the right ear and the vehicle w/o FITC (acetone:DBPTH) on the left ear. After 24 hrs. the thickness of each ear was measured, and to gauge the level of swelling/inflammation, the thickness of the left ear was compared to the FITC treated right ear. To assess the ability of the drug to block inflammation, the difference in R/L ear thickness were comparedfrom the mice that received FITC on the right ear, and drug vehicle (FITC/Vehicle group) to the group that received FITC on the right ear and either compound A (FITC/compound A) or dexamethasone (FITC/Dex). The control group only had vehicle (acetone:DBPTH) applied to the stomach area on days 1 & 2, and vehicle applied to both the right and left ears at the time of challenge. They also received the drug vehicle solution. The control animals did not mount a response to the vehicle (acetone:DBPTH) and did not have an increase in ear thickness compared to untreated animals.
2009-07-17 | E-TABM-521 | biostudies-arrayexpress