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  • br AKT signaling is essential during early dorsal patterning

    2024-02-09


    AKT signaling is essential during early dorsal patterning, neural crest induction and maturation
    AKT signaling modulates EMT and migration of the neural crest cells The defining feature of NC cells is their delamination from the dorsal neural epithelium. At the end of neurulation, mature premigratory NC cells lose their epithelial organization, acquire a mesenchymal morphology and emigrate from the neural tube towards multiple locations in the embryo. NCC modify their cell-cell contacts and cell-substratum adhesion properties, mediated notably by changes in the cadherins located at the plasma membrane and by modulation of integrin signaling (Mayor and Theveneau, 2013, Nieto et al., 2016). The NCC cytoskeleton is actively remodeled by a dynamic regulation of the ondansetron hcl 4mg network, allowing flexibility and fast morphology changes while the rhythm of cell divisions becomes coordinated with the constraints of cell migration (Nieto et al., 2016). During NC EMT and migration, the AKT pathway is involved in at least three of these cellular modifications: cytoskeleton changes, the stability of cell-cell junctions, and the nature of cell-substratum interactions in mouse, fish and frog embryos.
    AKT signaling promotes the differentiation of several NCC-derived lineages
    Conclusions and perspectives Recent studies highlight that the AKT signaling pathway is involved at all the steps of neural crest development, from establishment of the dorsal ectoderm and mesoderm during gastrulation to ectoderm regionalization and patterning of the neural border as well as for induction and maturation of the premigratory neural crest. AKT appears to play key cellular roles during these stages, including promoting EMT and migration, as well as for cell proliferation and survival during the differentiation of the neural crest derivatives. Because of this broad requirement for AKT activity, the experimental definition of AKT function at each individual step, in vivo, has required the use of time-controlled modulation of AKT signaling, e.g. using pharmacological agents, as well as by the use of tissue-specific spatial control of AKT activity with targeted strategies. In the developing embryo, the spatial and temporal dynamics of selected ligands and receptors orchestrates the fine-tuned activity of AKT. Specifically, in neural crest progenitors or tissues related to neural crest development, AKT signaling is activated and sustained in a tissue and time-specific manner by ligands binding RTKs or by non-conventional regulators, linked to the NC-GRN. For example, PDGFRα and PFKFB4 expression are controlled by NB/NC regulators (Figueiredo et al., 2017, Plouhinec et al., 2014). Collectively, these studies demonstrate that in the neural crest as in other cellular systems, AKT signaling is a hub potentially integrating the inputs from multiple pathways, and translating them into a coordinated cellular response, such as cell proliferation, survival, migration, or differentiation. In the neural crest context, it remains largely unknown which AKT effector(s) is (are) engaged to elicit each response. Comparison with adult cells or cancer cells with altered AKT response, which have been extensively studied could help us find the relevant effectors: for example, snai2, an essential transcription factor for neural crest induction and EMT initiation, is involved in migration and EMT of cancer such as melanoma, carcinoma or thyroid cancer (Fenouille et al., 2012, Julien et al., 2007, Visciano et al., 2015). Moreover, AKT is described to use TWIST1 to regulate cell migration in breast cancer and provide antiapoptotic properties in nasopharyngeal carcinoma cells (Li and Zhou, 2011, Zhang et al., 2007). Other potential AKT effectors from cancer studies, not yet recorded to participate in NC development could be identified by checking their expression at the different stages of NC formation in large-scale transcriptome studies (Plouhinec et al., 2017, Rabadán et al., 2013).