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Investigating the role of mechanosensing via PIEZO channels in neural crest derivatives

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216224%3A14110%2F25%3A00144444" target="_blank" >RIV/00216224:14110/25:00144444 - isvavai.cz</a>

  • Výsledek na webu

  • DOI - Digital Object Identifier

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Investigating the role of mechanosensing via PIEZO channels in neural crest derivatives

  • Popis výsledku v původním jazyce

    Neural crest is a transient population of cells formed during embryonic development that gives rise to multiple cell types, including mesenchymal cells, autonomic and sensory neurons, glia, and melanocytes. During morphogenesis, cells must respond to external cues, such as the mechanical properties of their microenvironment, to guide their migration and regulate their lineage commitment. Disruption in any of these processes can subsequently lead to developmental abnormalities and diverse disorders. However, the involvement of mechanical forces and mechanosensing in the development of neural crest-derived tissues still remains poorly understood. In this project, we explore the role of mechanosensing mediated by the mechanically gated ion channels PIEZO1 and PIEZO2 in neural crest derivatives in vivo. Using genetically engineered mouse models with tamoxifen-inducible double knockout of Piezo1 and Piezo2 in Sox10-expressing cells, we examine the effect of Piezo1/2 deletion during: (i) embryonic development and (ii) adult tissue homeostasis. We suggest that proper mechanosensing is essential for both the formation of neural crest-derived structures during embryogenesis and their maintenance during adulthood. Our work will provide new insights into how Piezo1/2 signalling shapes the structures of neural crest origin and contribute to a broader understanding of the role of mechanical forces in developmental biology.

  • Název v anglickém jazyce

    Investigating the role of mechanosensing via PIEZO channels in neural crest derivatives

  • Popis výsledku anglicky

    Neural crest is a transient population of cells formed during embryonic development that gives rise to multiple cell types, including mesenchymal cells, autonomic and sensory neurons, glia, and melanocytes. During morphogenesis, cells must respond to external cues, such as the mechanical properties of their microenvironment, to guide their migration and regulate their lineage commitment. Disruption in any of these processes can subsequently lead to developmental abnormalities and diverse disorders. However, the involvement of mechanical forces and mechanosensing in the development of neural crest-derived tissues still remains poorly understood. In this project, we explore the role of mechanosensing mediated by the mechanically gated ion channels PIEZO1 and PIEZO2 in neural crest derivatives in vivo. Using genetically engineered mouse models with tamoxifen-inducible double knockout of Piezo1 and Piezo2 in Sox10-expressing cells, we examine the effect of Piezo1/2 deletion during: (i) embryonic development and (ii) adult tissue homeostasis. We suggest that proper mechanosensing is essential for both the formation of neural crest-derived structures during embryogenesis and their maintenance during adulthood. Our work will provide new insights into how Piezo1/2 signalling shapes the structures of neural crest origin and contribute to a broader understanding of the role of mechanical forces in developmental biology.

Klasifikace

  • Druh

    O - Ostatní výsledky

  • CEP obor

  • OECD FORD obor

    10605 - Developmental biology

Návaznosti výsledku

  • Projekt

    <a href="/cs/project/GA25-18087S" target="_blank" >GA25-18087S: Buněčná podstata hojení zubu</a><br>

  • Návaznosti

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Ostatní

  • Rok uplatnění

    2025

  • Kód důvěrnosti údajů

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů