Xenbase Image ID: 148472

Fig. 5. A model of KCNQ1/KCNE1 function in embryogenesis. (A) A parsimonious model of the data proposes that KCNE1 modifies the function of KCNQ1, which up-regulates Sox10 and its downstream targets, such as XSlug. These factors are known to be necessary and sufficient for the observed up-regulation of proliferation, change in cell shape, and induction of invasive migration behavior in melanocytes. (B) Embryonic regions expressing KCNE1 induce up-regulation of key transcription factors, such as Sox10 and Slug, in other cells in the neural crest population, which confers upon them a hyperproliferative, invasive phenotype. This illustrates a non-cell-autonomous mechanism by which ion flows are transduced into canonical transcription cascades that control cell behavior. Black dashed lines indicate migration of hyperproliferating offspring of the target (green) cell. The original event takes place in the cell expressing KCNE1 (blue), which does not itself contribute all of the proliferative offspring. The target cell may induce the XSox10 pathway in neighbors by conventional biochemical signals (e.g., BMPs, FGFs, and WNTs). The direct biophysical interaction occurs in the target cell, where KCNE1-mediated loss of membrane polarization is relayed to the downstream signaling machinery by cell-autonomous mechanisms. Image published in: Morokuma J et al. (2008) Copyright © 2008. Image reproduced with permission of the publisher 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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