dc.contributor.advisor | Apidianakis, Yiorgos | en |
dc.contributor.author | Makris, Antreas | en |
dc.coverage.spatial | Cyprus | en |
dc.creator | Makris, Antreas | en |
dc.date.accessioned | 2024-05-27T04:58:36Z | |
dc.date.available | 2024-05-27T04:58:36Z | |
dc.date.issued | 2024-05 | |
dc.identifier.uri | http://gnosis.library.ucy.ac.cy/handle/7/66216 | en |
dc.description.abstract | Leaky Gut Syndrome is a condition characterised by increased intestinal permeability that may
lead to increased flow of lumen contents, such as nutrients, biomolecules, toxins, microbes, and
chemicals, into the bloodstream. Intestinal permeability may increase as a result of infection and
concomitant induction of intestinal regeneration. Here, we assessed the role of gut leakiness of genes
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expressed in the Drosophila midgut enteroendocrine cells (EEs) upon infection with Pseudomonas
aeruginosa. We found that downregulating Stumps/Dof or Lipin in the Drosophila midgut EEs leads to
a leaky gut. Stumps/Dof is an adaptor binding to the Fibroblast Growth Factor Receptor (FGFR).
Accordingly, the expression of a dominant-negative mutation of the FGFR in the midgut EEs leads to
a leaky gut. Interestingly, higher activity of the Drosophila FGFR in the EEs also leads to leaky gut.
This indicates that either overstimulation or suppression of FGFR signalling increases gut leakiness.
Lipin is a phosphatide phosphatase involved in lipid metabolism. Lipin inactivation via phosphorylation
is controlled by the insulin receptor (InR) in mammals. We found that InR downregulation in EEs does
not increase gut leakiness, but InR overexpression does, mimicking Lipin downregulation. Increased
leakiness upon Stumps/Dof and Lipin downregulation in EEs coincides with increased intestinal stem
cell (ISC) activity and improved survival upon infection, without any apparent effect on Armadillo
expression at the cell junctions. Moreover, Lipin downregulation changes EE density in the midgut,
while downregulation of Stumps/Dof does not. Thus, Lipin and Stumps/Dof act via different pathways
that converge in their ability to restrain midgut regeneration potential upon intestinal infection and
suppress midgut leakiness as a consequence | en |
dc.language.iso | eng | en |
dc.publisher | Πανεπιστήμιο Κύπρου, Σχολή Θετικών και Εφαρμοσμένων Επιστημών / University of Cyprus, Faculty of Pure and Applied Sciences | |
dc.rights | info:eu-repo/semantics/openAccess | en |
dc.title | Stumps and Lipin in the Drosophila midgut enteroendocrine cells independently regulate intestinal regeneration and permeability | en |
dc.type | info:eu-repo/semantics/masterThesis | en |
dc.contributor.committeemember | Georgiades, Pantelis | en |
dc.contributor.committeemember | Skourides, Paris A. | en |
dc.contributor.department | Πανεπιστήμιο Κύπρου, Σχολή Θετικών και Εφαρμοσμένων Επιστημών, Τμήμα Βιολογικών Επιστημών | el |
dc.contributor.department | University of Cyprus, Faculty of Pure and Applied Sciences, Department of Biological Sciences | en |
dc.subject.uncontrolledterm | DROSOPHILA | en |
dc.subject.uncontrolledterm | LEAKY GUT SYNDROME | en |
dc.subject.uncontrolledterm | CELL JUNCTIONS | en |
dc.subject.uncontrolledterm | ENTEROENDOCRINE CELLS (EEs) | en |
dc.subject.uncontrolledterm | INTESTINAL STEM CELLS (ISCs) | en |
dc.subject.uncontrolledterm | FIBROBLAST GROWTH FACTOR (FGF) SIGNALLING PATHWAY | en |
dc.subject.uncontrolledterm | INSULIN (IN) SIGNALLING PATHWAY | en |
dc.author.faculty | Σχολή Θετικών και Εφαρμοσμένων Επιστημών / Faculty of Pure and Applied Sciences | |
dc.author.faculty | Τμήμα Βιολογικών Επιστημών / Department of Biological Sciences | |
dc.type.uhtype | Master Thesis | en |
dc.rights.embargodate | 2028-05-31 | |
dc.contributor.orcid | Apidianakis, Yiorgos [0000-0002-7465-3560] | |
dc.contributor.orcid | Georgiades, Pantelis [0000-0002-5538-3163] | |
dc.contributor.orcid | Skourides, Paris A. [0000-0003-3502-5729] | |
dc.rights.embargoreason | Publication | en |
dc.gnosis.orcid | 0000-0002-7465-3560 | |
dc.gnosis.orcid | 0000-0002-5538-3163 | |
dc.gnosis.orcid | 0000-0003-3502-5729 | |