Embigin as a regulator of mouse embryonic development
Talvi, Salli (2025-11-28)
Embigin as a regulator of mouse embryonic development
Talvi, Salli
(28.11.2025)
Turun yliopisto
Julkaisun pysyvä osoite on:
https://urn.fi/URN:ISBN:978-952-02-0437-2
https://urn.fi/URN:ISBN:978-952-02-0437-2
Kuvaus
navigointi mahdollista
kuvilla vaihtoehtoiset kuvaukset
taulukot saavutettavia
looginen lukemisjärjestys
kuvilla vaihtoehtoiset kuvaukset
taulukot saavutettavia
looginen lukemisjärjestys
Tiivistelmä
Embigin (Gp70) is a transmembrane glycoprotein belonging to the basigin subgroup of the immunoglobulin superfamily. Embigin functions as an ancillary protein for monocarboxylate transporters (MCT) and may regulate cell-extracellular matrix interactions, particularly through fibronectin. Additionally, in adult mice, embigin function has been linked to stem cell regulation. However, the role of embigin in mouse embryogenesis has remained unclear. This doctoral thesis describes embigin protein expression during embryogenesis and in adult mice and the effect of embigin deficiency (Emb-/-) in mice, especially in lung and kidney organogenesis, and sheds some light on the function of embigin during mouse development.
First, we found that embigin protein is highly expressed during the early stages of mouse embryogenesis and later in the tubular epithelial structures of the lungs, kidneys, epididymis, and skin. The high neonatal mortality observed in Emb-/- mice is mainly due to delayed lung maturation and general delayed embryonic development. We noticed embigin expression in the lung primordium, suggesting the function of embigin is vital during early lung development. Furthermore, embigin was detected in adult mouse lungs in stem-like club cells. Second, we described in detail the protocol for the lung branching analysis in E12.5 mouse embryos used in the first article. Third, during mouse kidney development, we found that embigin is expressed in the kidney primordium and later in the ureteric bud (UB) and differentiating nephron precursors. The embigin deficiency retards UB branching during the early stages of kidney development, and in E13.5 Emb-/- kidneys, genes related to nephron development were downregulated. However, the observed delay was transient. Additionally, embigin appears to regulate directly Pappa2, Acta2, and Tagln genes during kidney development. Overall, embigin likely participates in early mouse development by supporting tissue-specific stem cell functions.
First, we found that embigin protein is highly expressed during the early stages of mouse embryogenesis and later in the tubular epithelial structures of the lungs, kidneys, epididymis, and skin. The high neonatal mortality observed in Emb-/- mice is mainly due to delayed lung maturation and general delayed embryonic development. We noticed embigin expression in the lung primordium, suggesting the function of embigin is vital during early lung development. Furthermore, embigin was detected in adult mouse lungs in stem-like club cells. Second, we described in detail the protocol for the lung branching analysis in E12.5 mouse embryos used in the first article. Third, during mouse kidney development, we found that embigin is expressed in the kidney primordium and later in the ureteric bud (UB) and differentiating nephron precursors. The embigin deficiency retards UB branching during the early stages of kidney development, and in E13.5 Emb-/- kidneys, genes related to nephron development were downregulated. However, the observed delay was transient. Additionally, embigin appears to regulate directly Pappa2, Acta2, and Tagln genes during kidney development. Overall, embigin likely participates in early mouse development by supporting tissue-specific stem cell functions.
Kokoelmat
- Väitöskirjat [3042]
