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Published on: December 12, 2014
PTK7: a cell polarity receptor with multiple facets
Anne-Catherine Lhoumeau1, Francesca Puppo, Thomas Prébet
1INSERM U891, Centre de Recherche en Cancérologie de Marseille, Marseille, France.
Abstract:
PTK7 is a tyrosine kinase receptor implicated in planar cell polarity, a process with multiple implications at the cellular and organism levels. Loss of function of PTK7 leads to profound morphogenetic defects in the mouse, such as neural tube defects, misorientation of stereocilia in the inner ear, and impaired polarized cell movements. The planar cell polarity pathway is classically assigned to a non-canonical Wnt pathway, which does not rely on b-catenin transcriptional activity. We recently revealed that PTK7 is implicated in b-catenin-dependent developmental processes in mammalian and Xenopus systems. Based on data recently obtained by our group as well as others, we discuss how PTK7 could be involved in canonical and non-canonical Wnt pathways, and which implications are expected from these data in physiology and physiopathology.
Insights
Protein tyrosine kinase 7 (PTK7) plays a crucial role in cell polarity and development. Our findings reveal PTK7
Area of Science:
- Developmental Biology
- Cell Signaling
- Molecular Biology
Background:
- Planar cell polarity (PCP) is essential for tissue morphogenesis and organ development.
- PTK7, a tyrosine kinase receptor, is known to regulate PCP.
- Classical PCP pathways are often considered independent of beta-catenin.
Purpose of the Study:
- To investigate the role of PTK7 in beta-catenin-dependent signaling.
- To explore PTK7's involvement in both canonical and non-canonical Wnt pathways.
- To understand the physiological and pathophysiological implications of PTK7 function.
Main Methods:
- Utilizing mammalian and Xenopus model systems.
- Analyzing genetic loss-of-function data.
- Integrating recent experimental findings from multiple research groups.
Main Results:
- PTK7 loss-of-function causes significant morphogenetic defects, including neural tube defects.
- PTK7 is implicated in beta-catenin-dependent processes.
- Evidence suggests PTK7 integrates into both canonical and non-canonical Wnt signaling.
Conclusions:
- PTK7 is a key regulator linking PCP to beta-catenin-dependent pathways.
- Understanding PTK7's dual role in Wnt signaling is critical for developmental processes.
- Dysregulation of PTK7 may contribute to various pathophysiological conditions.
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