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Fig. 8. Summary model of Vmem/pH-dependent signaling. A: The three courses of electrophysiological activity (Fig. 2). At approximately stage 18, a consistent pattern appears: depolarized neural folds (darker), hyperpolarized lateral ectoderm (brighter). B: A typical wildtype stage-18 embryo. The pattern shown here for Vmem compartments matches the pattern seen for pH compartments at the same stage. Drawings illustrate our model. The Vmem and pH of the SE cells, labeled 1 in the drawing, influence gene expression in the nearby deep cells, labeled 5. The electrophysiological state of the SE cell can influence the genes of the deep cell by various mechanisms, (1 ,2 , 3, and 4). Secretion of signaling molecules can be affected by the HV-ATPase-dependent control of vesicle pH (1), consistent with Cruciat (2010). Proteins on the surface of the SE cell (2) can be voltage or pH gated; many only function in a narrow range of pH or Vmem. The pH of the intercellular space (2), would also affect diffusible signaling molecules, or the receptors on the surface of the deep cells (3), by the same mechanism. After reaching the surface of the deep cell, the signal could be carried to the nucleus by any of a myriad of signaling pathways. We also hypothesize that the bioelectric signal originating in the SE cells affects the mechanical state of the cells. One hypothesis is that changes in Vmem open voltage-gated Ca2+ channels (3), leading to Ca2+-dependent changes in the cytoskeleton (4), an important player in cell shape change and invagination. Another possibility is that Vmem changes trigger voltage-gated ion channels (3), causing ion and thus water efflux, changing the osmotic pressure of the cells, and thus their resistance to shape change. This is consistent with our observation that cells expressing abnormally high amounts of xfz3 often appear larger.

Image published in: Vandenberg LN et al. (2011)

Copyright © 2011. Image reproduced with permission of the Publisher, John Wiley & Sons.

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