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COVER PICTURE:
Early developing thymocytes depend on the cytoprotective functions of survivin for continued survival and proliferation. In the absence of survivin, proteins essential for spindle formation in cycling thymocytes are mislocalized, constituting "cell damage." Some survivin-deficient thymocytes activate the tumor suppressor p53, which induces cell cycle arrest at G1 via activation of the downstream effector p21. Cells taking this path eventually succumb to senescence. However, the spindle defects in other cycling survivin-deficient thymocytes precipitate a form of cell death resembling mitotic catastrophe. Strikingly, this form of cell death is independent of p53 and cannot be rescued by Bcl-2. See related article by Okada et al., pp. 399-410. Cover art by Graham Hutcheson.
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