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Dying Cells Promote Proliferation

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Science's STKE  03 Aug 2004:
Vol. 2004, Issue 244, pp. tw279-TW279
DOI: 10.1126/stke.2442004TW279

Huh et al. used the developing Drosophila wing to study whether activation of the apoptotic pathway, while preventing cell death by inhibition of effector caspase activity, would stimulate proliferation of adjacent cells. The impetus for this experiment was the observation that even if more than half of the cells in the wing disc are lost, the wing disc cells will compensate and will proliferate enough to replace the missing cells and to produce a normal-sized wing. In cells of the posterior wing compartment, the cell death pathway was activated by expression of head involution defective (Hid), at the same time that cell death was prevented by expression of the baculovirus p35 protein, which inhibits effector caspase activity (but not activation). When Hid and p35 were both present, there were increased numbers of cells in the posterior wing compartment compared with those in the absence of the two proteins or in the presence of p35 alone. When a dominant-negative form of the caspase Dronc was also introduced with p35 and Hid, the overproliferation response was blocked. Analysis of wings with clones of tissue expressing p35 and Hid showed increased proliferation in the area adjacent to the clones, but not of the clonal cells themselves. Thus, dying cells may transmit a signal through a Dronc-dependent mechanism that stimulates neighboring cells to allow for compensatory cell proliferation.

J. R. Huh, M. Guo, B. A. Hay, Compensatory proliferation induced by cell death in the Drosophila wing disc requires activity of the apical cell death caspase Dronc in a nonapoptotic role. Current Biol. 14, 1262-1266 (2004). [Online Journal]

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