Our simple model is consistent with experimental probes of mitochondrial and cellular variability.

<p>Comparison between our model (red) and experimental data (blue), following discussion in the Main Text. <b>Experimental data from das Neves </b><b><i>et al.</i></b><b> </b><a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1002416#pcbi.1002416-dasNeves1" target="_blank">[<b>31</b>]</a><b>.</b> A. Distribution of mitochondrial mass in an unsynchronised population of cells. B. Distribution of cell volume in an unsynchronised population of cells. C. Comparison of the lengths of cell cycles between generations: Gen 1 is the parent cell, Gen 2 the daughter. Cell cycle lengths are only weakly correlated. D. Relationship between the ratio of mitochondrial masses at birth against ratio of cell cycle lengths for sister pairs. E. Relationship between the ratio of cellular volumes at birth and the ratio of cell cycle lengths for sister pairs, showing a weaker correlation than D. F. Transcription rate noise in subsets of the population in , , and phases (see Main Text). G. Mitochondrial mass and cell volume are strongly correlated in our model. Some experimental evidence is contradictory (see Main Text). H. Distribution of transcription rate per unit volume . <b>New experimental data (see </b><a href="http://www.ploscompbiol.org/article/info:doi/10.1371/journal.pcbi.1002416#s4" target="_blank"><b>Methods</b></a><b>).</b> I. Distribution of total mitochondrial functionality ( in our model, CMXRos readings from experiments). J. Mean and standard deviation of cell cycle lengths in (A)nti-oxidant-treated, (C)ontrol, and (P)ro-oxidant-treated populations. Experimental histograms, originally presented in arbitrary units, have been scaled to match the mean value of the simulated data.