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Published 25 October 2004. doi:10.1083/jcb.200406073
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 167, Number 2, 303-313
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Article

 Decreased apoptosome activity with neuronal differentiation sets the threshold for strict IAP regulation of apoptosis

Kevin M. Wright1, Michael W. Linhoff2, Patrick Ryan Potts2, and Mohanish Deshmukh2

1 Curriculum in Neurobiology, University of North Carolina, Chapel Hill, NC 27599
2 Neuroscience Center and the Department of Cell and Developmental Biology, University of North Carolina, Chapel Hill, NC 27599

Correspondence to Mohanish Deshmukh: mohanish{at}med.unc.edu

Despite the potential of the inhibitor of apoptosis proteins (IAPs) to block cytochrome c–dependent caspase activation, the critical function of IAPs in regulating mammalian apoptosis remains unclear. We report that the ability of endogenous IAPs to effectively regulate caspase activation depends on the differentiation state of the cell. Despite being expressed at equivalent levels, endogenous IAPs afforded no protection against cytochrome c–induced apoptosis in naïve pheochromocytoma (PC12) cells, but were remarkably effective in doing so in neuronally differentiated cells. Neuronal differentiation was also accompanied with a marked reduction in Apaf-1, resulting in a significant decrease in apoptosome activity. Importantly, this decrease in Apaf-1 protein was directly linked to the increased ability of IAPs to stringently regulate apoptosis in neuronally differentiated PC12 and primary cells. These data illustrate specifically how the apoptotic pathway acquires increased regulation with cellular differentiation, and are the first to show that IAP function and apoptosome activity are coupled in cells.

Abbreviations used in this paper: E16, embryonic day 16; IAP, inhibitor of apoptosis protein; P5, postnatal day 5; PC12, pheochromocytoma.


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