Skew or third moment of bacterial generation times

Abstract

We studied two statistical hypotheses for the occurrence of cellular division and compared these hypotheses to available data. The two models were tested by observed distributions of cellular size during steady-state growth. The 30-year-old sloppy size model could be rejected, whereas the recently developed incremental size proposal could not. The latter proposition was accepted by default. We concluded that the time between successive divisions is not simply derived from extant size at cellular division, but rather from interdivisional size increment. We therefore propose that cellular division is regulated by the need of cells at birth to accumulate a certain amount of mass or something related to mass before division.

Membranes, energetics, and evolution across the prokaryote-eukaryote divide

“…Second, only a fraction of bacterial membranes appears to be allocated to bioenergetic functions (Magalon and Alberge, 2016), again shedding doubt on whether membrane area is a limiting factor for energy production. Third, in every bacterial species for which data are available, growth in cell volume is close to exponential, that is, the growth rate of a cell increases as its cell volume increases despite the reduction in the surface area:volume ratio (Voorn and Koppes, 1998; Godin et al, 2010; Santi et al, 2013; Iyer-Biswas et al, 2014; Osella et al, 2014; Campos et al, 2014). …”

A Constant Size Extension Drives Bacterial Cell Size Homeostasis

“…Our data show that while there is significant fluctuations in Δ L values, cells elongate, on average , a constant amount before dividing, irrespective of their length at birth (Figure 1G, H, Figure 2F, and Figure S2). A constant elongation — or the addition of a volume increment — can, at least theoretically, lead to cell size homeostasis (Amir, 2014; Voorn and Koppes, 1998). Figure 3A shows schematically how a constant length extension followed by a symmetric division can compensate for cell size fluctuations within a few generations.…”

“…These alternative mechanisms include a molecular clock, a simple timer, the addition of a constant cell volume, transition probability, or a concerted ‘sloppy’ sizer and timer (Fantes and Nurse, 1981; Osella et al, 2014). For example, based on mathematical modeling, Voorn and Koppes first (1998), and Amir later (2014) argued that addition of a constant volume at each generation can describe the experimental shape of bacterial cell size distributions as well as population-derived bulk correlations (the positive correlation in size between mothers and daughters and the negative correlation between cell cycle time and size at birth). However, these statistical features have alternative explanations (Hosoda et al, 2011; Osella et al, 2014) and can be described by sizer-based homeostasis mechanisms (Koch and Schaechter, 1962; Koppes et al, 1980; Robert et al, 2014; Turner et al, 2012).…”

Cell-Shape Homeostasis in Escherichia coli Is Driven by Growth, Division, and Nucleoid Complexity

“…As is common in biological systems, the variance of celllength distribution at later stages is anticipated to be larger, but the variation at division is smaller than those at earlier events in the cycle (18). Koppes et al (19) proposed that cells initiate constriction after a constant length increment after initiation of DNA replication or between two successive divisions (20). A recent surge of articles (21-24) resurrects this old question; analyses of high throughput results suggest that a steady-state growing culture maintains a stable size distribution by adding a constant, growth-ratedependent, mean incremental length DL, which is equal to the mean length of a newborn cell L b , each generation irrespective of its real size at birth.…”