Non-genetic origins of cell-to-cell variability in TRAIL-induced apoptosis

Sabrina L. Spencer, Suzanne Gaudet, John G. Albeck, John M. Burke and Peter K. Sorger ()
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Sabrina L. Spencer: Center for Cell Decision Processes, Harvard Medical School, Boston, Massachusetts 02115, USA
Suzanne Gaudet: Center for Cell Decision Processes, Harvard Medical School, Boston, Massachusetts 02115, USA
John G. Albeck: Center for Cell Decision Processes, Harvard Medical School, Boston, Massachusetts 02115, USA
John M. Burke: Center for Cell Decision Processes, Harvard Medical School, Boston, Massachusetts 02115, USA
Peter K. Sorger: Center for Cell Decision Processes, Harvard Medical School, Boston, Massachusetts 02115, USA

Nature, 2009, vol. 459, issue 7245, 428-432

Abstract: Apoptosis: an explanation for 'fractional killing'? Noisy gene expression or unequal partition of molecules during cell division are increasingly recognized as key sources of non-genetic cell-to-cell heterogeneity but the consequences for disease progression and drug efficiency are little understood. Through single-cell imaging, Spencer et al. now show that pre-existing cell-to-cell differences in the levels of signalling proteins determine whether the addition of an external death signal will kill a cell by apoptosis or not — and how quickly it happens. The mechanism may explain the phenomenon of 'fractional killing', in which repeated rounds of chemotherapy kill some but not all cells in a tumour. From an evolutionary perspective, such systems-level phenotypic variation — not based on genetic or epigenetic modifications — offers wider adaptive potential to populations of living organisms.

Date: 2009
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DOI: 10.1038/nature08012

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