Caspase-2 activation in the absence of PIDDosome formation

Journal of Cell Biology - Tập 185 Số 2 - Trang 291-303 - 2009
Claudia Manzl1, Gerhard Krumschnabel1, Florian Bock1, Bénédicte Sohm1, Verena Labi1, Florian Baumgartner1, Emmanuelle Logette2, Jürg Tschopp2, Andreas Villunger1
1Division of Developmental Immunology, Biocenter, Innsbruck Medical University, A-6020 Innsbruck, Austria 1
2Department of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland 2

Tóm tắt

PIDD (p53-induced protein with a death domain [DD]), together with the bipartite adapter protein RAIDD (receptor-interacting protein-associated ICH-1/CED-3 homologous protein with a DD), is implicated in the activation of pro–caspase-2 in a high molecular weight complex called the PIDDosome during apoptosis induction after DNA damage. To investigate the role of PIDD in cell death initiation, we generated PIDD-deficient mice. Processing of caspase-2 is readily detected in the absence of PIDDosome formation in primary lymphocytes. Although caspase-2 processing is delayed in simian virus 40–immortalized pidd−/− mouse embryonic fibroblasts, it still depends on loss of mitochondrial integrity and effector caspase activation. Consistently, apoptosis occurs normally in all cell types analyzed, suggesting alternative biological roles for caspase-2 after DNA damage. Because loss of either PIDD or its adapter molecule RAIDD did not affect subcellular localization, nuclear translocation, or caspase-2 activation in high molecular weight complexes, we suggest that at least one alternative PIDDosome-independent mechanism of caspase-2 activation exists in mammals in response to DNA damage.

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Journal of Cell Biology

Tập 185 Số 2

291-303

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