When a hydra is decapitated, the Wnt pathway is activated in the apical portion that will form a new head. If the cut is made just below the hypostome, Wnt3 is upregulated in the epithelial cells near the cut surface, which causes the remodeling of existing cells to form the head. No proliferation is seen in this case; hence, it is morphallactic regeneration (regeneration by cell transdifferentiation). If the hydra is cut at its midsection, however, the cells derived from the interstitial stem cell (neurons, nematocytes, secretory cells, and gametes) undergo apoptosis immediately below the cut site. Before dying, however, these cells produce a burst of Wnt3, which activates β-catenin in the interstitial cells beneath them. This β-catenin surge causes a wave of proliferation in the interstitial cells as well as remodeling in the epithelial cells. Here we have epimorphosis or epimorphic regeneration (regeneration by cell dedifferentiation) (Chera et al. 2009). Canonical Wnt signaling is thus important both in normal budding and in head regeneration.
In hydra, if a midsection cut and a more apical cut both result in Wnt activation, how is apoptosis triggered in the first scenario but not in the other?
Chera, S., L. Ghila, K. Dobretz, Y. Wenger, C. Bauer, W. Buzgariu, J. C. Martinou and B. Galliot. 2009. Apoptotic cells provide an unexpected source of Wnt3 signaling to drive Hydra head regeneration. Dev. Cell 17: 279–289.
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