RNA sequencing of the Murine Oviduct Infundibulum
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE199199 | GEO | 2022/04/30
REPOSITORIES: GEO
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Project description:Ciliary action performs a critical role in the oviduct (Fallopian tube), during pregnancy establishment through sperm and egg transport. The disruption of normal ciliary function in the oviduct affects oocyte pick-up and is a contributing factor to female infertility. Estrogen is an important regulator of ciliary action in the oviduct and promotes ciliogenesis in several species. Global loss of estrogen receptor 1 alpha (encoded by Esr1 gene) leads to infertility. Our laboratory has previously shown that ESR1 in the oviductal epithelial cell layer is required for female fertility. Here, we assessed the role of estrogen on transcriptional regulation of ciliated epithelial cells of the oviduct using single-cell RNA-sequencing analysis. We observed minor variations in ciliated cell genes in the proximal region (isthmus and uterotubal junction) of the oviduct. However, E2 treatment had little impact on the gene expression profile of ciliated epithelial cells. To assess the requirement of ESR1 specifically in ciliated cells for female fertility, we conditionally ablated Esr1 from ciliated epithelial cells of the oviduct (called ciliated Esr1d/d mice). Our studies showed that ciliated Esr1d/d females had fertility rates comparable to control females, did not display any disruptions in preimplantation embryo development or embryo transport to the uterus, and had comparable cilia formation to control females. However, we observed some incomplete deletion of Esr1 in the ciliated epithelial cells, especially in the ampulla region. Therefore, more studies are required to definitively determine ESR1 function in ciliated cells of the oviduct. Nevertheless, our data suggest that ESR1 expression in ciliated cells of the oviduct is dispensable for ciliogenesis, but nonessential for female fertility in mice. All genes expressed in scRNA-seq datasets are available for scientific community and separable at https://www.winuthayanon.com/genes/ve2h_cilia/ and https://www.winuthayanon.com/genes/ve2h_allclusters/
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Project description:Cilia are ubiquitous cell surface projections that modulate various sensory- and motility based processes and are implicated in a growing number of multi-organ genetic disorders termed ciliopathies. As new components required for cilium biogenesis and function remain unidentified, we sought to further define and validate the transcriptional targets of the ciliogenic C. elegans RFX transcription factor DAF-19. To this end, transcriptional profiling of daf-19 mutants (which do not form cilia) and wild-type animals was performed using selectively staged embryos where ciliogenesis occurs in most ciliated sensory neurons (CSNs). Statistical comparisons between the two populations revealed 881 differentially regulated genes with 1.5-fold change or greater. A subset of these was confirmed by quantitative RT-PCR. Transgenic worms expressing transcriptional-GFP fusions revealed CSN-specific expression patterns for 9 of 12 candidate genes. We show that two uncharacterized candidate genes, which we term dyf-17 and dyf-18 because their corresponding mutants display dye-filling (Dyf) defects, are important for ciliogenesis. DYF-17 localizes at the base of cilia and interestingly, is specifically required for building the distal segment of sensory cilia. DYF-18 is an evolutionarily conserved CDK-7/CCRK-related serine-threonine kinase that is necessary for the proper function of intraflagellar transport (IFT), a process critical for cilium biogenesis. Together, our comparative microarray study identifies targets of the evolutionarily conserved RFX transcription factor, DAF-19, providing a rich dataset from which to uncover—in addition to DYF-17 and DYF-18—cellular components important for cilium formation and function. 4 daf-19,daf12; 4 daf-12; 4 WT
2011-07-25 | E-GEOD-25633 | biostudies-arrayexpress
Project description:Prolong elevation of prolactin and sex-depnendt regulation of pain chronicity
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Project description:This a model from the article:
Mathematical modelling of prolactin-receptor interaction and the corollary for prolactin receptor gene expression in skin
Soboleva TK, Vetharaniam I, Nixon AJ, Montenegro R, Pearson AJ, Sneyd J. J Theor Biol.
(2005) 234(2); 289-98 15757685
,
Abstract:
A mathematical model of prolactin regulating its own receptors was developed, and compared with experimental data on a qualitative level. The model incorporates the kinetics of prolactin-receptor interactions and subsequent signalling by prolactin-receptor dimers to regulate the production of receptor mRNA and hence the receptor population. The model relates changes in plasma prolactin concentration to prolactin receptor (PRLR) gene expression, and can be used for predictive purposes. The cell signalling that leads to the activation of target genes, and the mechanisms for regulation of transcription, were treated empirically in the model. The model's parameters were adjusted so that model simulations agreed with experimentally observed responses to administration of prolactin in sheep. In particular, the model correctly predicts insensitivity of receptor mRNA regulation to a series of subcutaneous injections of prolactin, versus sensitivity to prolonged infusion of prolactin. In the latter case, response was an acute down-regulation followed by a prolonged up-regulation of mRNA, with the magnitude of the up-regulation increasing with the duration of infusion period. The model demonstrates the feasibility of predicting the in vivo response of prolactin target genes to external manipulation of plasma prolactin, and could provide a useful tool for identifying optimal prolactin treatments for desirable outcomes.
This model was taken from the CellML repository
and automatically converted to SBML.
The original model was:
soboleva, vetharaniam, nixon, montenegro, pearson, sneyd, 2005, version01
The original CellML model was created by:
Lloyd, Catherine, May
c.lloyd(at)auckland.ac.nz
The University of Auckland
Auckland Bioengineering Institute
This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team.
To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication
for more information.
In summary, you are entitled to use this encoded model in absolutely any manner you deem suitable, verbatim, or with modification, alone or embedded it in a larger context, redistribute it, commercially or not, in a restricted way or not..
To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.
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Project description:Influenza B virus (IBV) is an acute respiratory pathogen that induces phenotypic alterations to the lung epithelium, such as the denudation of the respiratory cilium, during and after IBV infection. It has been assumed that these epithelial changes are non-adaptive, and simply the result of cellular death following lytic virus infection. However, previous reports have shown that not all infected cells are killed after viral infection; some cells can completely clear viral RNA and protein and persist in the host long-term. In this study, we utilized a novel recombinant virus in combination with a Cre recombinase-responsive transgenic mouse model to demonstrate that IBV infection leads to the formation of a population of survivor ciliated cells in the proximal airways of infected mice. To ensure that we were studying ciliated cells with markers that were maintained during viral infection in vivo, we performed single-cell transcriptional profiling on infected and surviving ciliated cell populations. We digested mouse lungs and sorted cells using tdTomato as a marker of infection. We sorted cell populations from the lungs of animals mock infected with PBS (Mock) and during active infection (2 DPI). The resulting data revealed that the marker CD24 is consistently expressed on ciliated cells before and during viral infection.
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Project description:Influenza B virus (IBV) is an acute respiratory pathogen that induces phenotypic alterations to the lung epithelium, such as the denudation of the respiratory cilium, during and after IBV infection. It has been assumed that these epithelial changes are non-adaptive, and simply the result of cellular death following lytic virus infection. However, previous reports have shown that not all infected cells are killed after viral infection; some cells can completely clear viral RNA and protein and persist in the host long-term. In this study, we utilized a novel recombinant virus in combination with a Cre recombinase-responsive transgenic mouse model to demonstrate that IBV infection leads to the formation of a population of survivor ciliated cells in the proximal airways of infected mice. We then performed transcriptional profiling on infected and surviving ciliated cell populations to determine how surviving viral infection affected these cells. To specifically profile ciliated cells, we digested mouse lungs and sorted cells based on their expression of CD24 with tdTomato as a marker of infection. We sorted cell populations from the lungs of animals mock infected with PBS (Mock), during active infection (2 DPI), and matched ciliated cell populations at 14 days post-infection that had either experienced direct viral infection (14 DPI Survivor Cell) or those that had never been infected (14 DPI). The resulting data indicate that after surviving infection and clearing the virus, survivor ciliated cells undergo significant transcriptional reprogramming.
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