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Apoptosis is essential for numerous processes, such as development,resistance to infections, and suppression of tumorigenesis. Here, weinvestigate the influence of the nutrient sensing and longevity-assuring enzymeSIRT6 on the dynamics of apoptosis triggered by serum starvation. Specifically,we characterize the progression of apoptosis in wild type and SIRT6 deficientmouse embryonic fibroblasts using time-lapse flow cytometry and computationalmodelling based on rate-equations and cell distribution analysis. We find thatSIRT6 deficient cells resist apoptosis by delaying its initiation.Interestingly, once apoptosis is initiated, the rate of its progression ishigher in SIRT6 null cells compared to identically cultured wild type cells.However, SIRT6 null cells succumb to apoptosis more slowly, not only inresponse to nutrient deprivation but also in response to other stresses. Ourdata suggest that SIRT6 plays a role in several distinct steps of apoptosis.Overall, we demonstrate the utility of our computational model to describestages of apoptosis progression and the integrity of the cellular membrane.Such measurements will be useful in a broad range of biological applications.We describe a computational method to evaluate the progression of apoptosisthrough different stages. Using this method, we describe how cells devoid ofSIRT6 longevity gene respond to apoptosis stimuli, specifically, how theyrespond to starvation. We find that SIRT6 cells resist apoptosis initiation;however, once initiated, they progress through the apoptosis at a faster rate.These data are first of the kind and suggest that SIRT6 activities might playdifferent roles at different stages of apoptosis. The model that we propose canbe used to quantitatively evaluate progression of apoptosis and will be usefulin studies of cancer treatments and other areas where apoptosis is involved.

SIRT6 Knockout Cells Resist Apoptosis Initiation but Not Progression: A Computational Method to Evaluate the Progression of Apoptosis