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Figure 8. Hypothetical model to depict the role of Trpc1 channels in linking the inhibition of BMP pathway by noggin, and the activation of Cav1.2 channels in ectodermal cells. During gastrulation, the cells of the embryonic ectoderm have the choice between two fates; they can give rise to either epidermal or neural progenitors. In the plasma membrane, the molecular components involved in this choice are BMP receptors type I (BmprI) and type II (BmprII), Trpc1 and voltage-dependent Ca2+ channels (Cav1.2). The membrane potential in the ectoderm is ~−60 mV; i.e., the interior is negatively charged62. (A) Induction of the epidermis occurs through a signalling cascade, which involves the binding of Bmp4 to its receptor, and then the transphosphorylation of BmprII by BmprI. This is followed by the activation of Smads, which translocate into the nucleus to form active transcriptional complexes to control the expression of epidermal genes. In this scenario, there is no interaction between Trpc1 and BmprII, and Cav1.2 remains inactive. (B) During neural induction, noggin binds to BMP4, and thus prevents the activation of the BMP pathway. As a consequence, it induces a physical interaction between BmprII and Trpc1 channels. This interaction leads to the activation of Trpc1, which either alone or associated with other Trp channels (e.g., Trpv4), triggers an influx of cations (Ca2+ and Na+). This influx of cations depolarizes the membrane (i.e., there is more positive charge inside) up to a threshold sufficient to open the voltage-gated Ca2+ channel, Cav1.2. As we have previously shown27,29, the resulting influx of Ca2+ is then sufficient to activate the expression. Image published in: Néant I et al. (2019) © The Author(s) 2019. This image is reproduced with permission of the journal and the copyright holder. This is an open-access article distributed under the terms of the Creative Commons Attribution license Larger Image Printer Friendly View

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