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PTK7 signaling complexes in neural crest cell migration
Cell migration is an important process during embryonic development and is strongly regulated by external signals, both chemical and mechanical. Neural crest (NC) cells are highly migratory cells, which are ideal for analyzing cell migration due to their high similarities to cancer cells. NC cells a...
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| Format: | Daten Dissertation |
| Sprache: | Englisch |
| Veröffentlicht: |
Philipps-Universität Marburg
2019
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| Online Zugang: | Datensatz ansehen PDF-Volltext |
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| Zusammenfassung: | Cell migration is an important process during embryonic development and is strongly regulated by external signals, both chemical and mechanical. Neural crest (NC) cells are highly migratory cells, which are ideal for analyzing cell migration due to their high similarities to cancer cells. NC cells are induced at the border region of the neural folds and migrate along the anterior-posterior axis through the embryo. The NC cells have the ability to penetrate mesenchymal and ectodermal tissue but do not penetrate other NC cells, regulated by a process called contact inhibition of locomotion (CIL). CIL describes the process in which cells change their migration direction after contact with another cell. The non-canonical Wnt pathway is important for this process. Upon activation of the non-canonical Wnt pathway, the Frizzled receptor recruits the cytoplasmic protein Dishevelled to the membrane. This leads to activation of small GTPases and reorganization of the actin cytoskeleton. The transmembrane protein PTK7 (protein tyrosine kinase 7) is an activator of the non-canonical Wnt signaling pathway and expressed in NC cells. This study shows that in migrating NC cells PTK7, mediated by its extracellular domain, accumulates at cell-cell contact sites. A loss of function of PTK7 in Xenopus leads to an inhibition of NC cell migration. However, the role of PTK7 signaling during NC cell migration remains to be analyzed. During this study it has been shown that PTK7 loss of function leads to alteration of NC cell morphology and thereby inhibition of NC cell migration. This NC cell migration defects can be rescued by overexpression of Dishevelled. In addition, a new interaction partner was identified. The Rho guanine nucleotide exchanging factor Trio interacts with PTK7, co-localizes with PTK7 in NC cells and an overexpression of Trio rescues PTK7 loss of function defects in NC cell migration. In summary, this work has provided further insight into the PTK7 signaling pathway during NC cell migration. |
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| Umfang: | 108 Seiten |
| DOI: | 10.17192/z2019.0518 |