Abstract
The decision to divide is the most important one that any cell must make. Recent single cell studies suggest that most bacteria follow an “adder” model of cell size control, incorporating a fixed amount of cell wall material before dividing. Mycobacteria, including the causative agent of tuberculosis Mycobacterium tuberculosis, are known to divide asymmetrically resulting in heterogeneity in growth rate, doubling time, and other growth characteristics in daughter cells. The interplay between asymmetric cell division and adder size control has not been extensively investigated. Moreover, the impact of changes in the environment on growth rate and cell size control have not been addressed for mycobacteria. Here, we utilize time-lapse microscopy coupled with microfluidics to track live Mycobacterium smegmatis cells as they grow and divide over multiple generations, under a variety of growth conditions. We demonstrate that, under optimal conditions, M. smegmatis cells robustly follow the adder principle, with constant added length per generation independent of birth size, growth rate, and inherited pole age. However, the nature of the carbon source induces deviations from the adder model in a manner that is dependent on pole age. Understanding how mycobacteria maintain cell size homoeostasis may provide crucial targets for the development of drugs for the treatment of tuberculosis, which remains a leading cause of global mortality.
Highlights
Bacteria have long been known to maintain their average size within steady state populations, but we do not yet have a full mechanistic understanding of how this is achieved (Chien et al, 2012)
Cell size homoeostasis and its interplay with gene expression and growth is of critical importance for bacterial survival, since the requirement for additional space to incorporate nascent DNA and to subsequently permit cell division must be balanced with the necessity to maintain the concentration of critical proteins, such as those involved in metabolism or protein synthesis (Shahrezaei and Marguerat, 2015)
These strategies and their molecular mechanisms are beginning to be investigated in detail at the single cell level, Cell Size Control in Mycobacteria especially with model bacterial species such as Escherichia coil and Caulobacter crescentus (Campos et al, 2014; Taheri-Araghi et al, 2015) but how these principles apply to other bacterial systems such as mycobacteria is less well understood
Summary
Bacteria have long been known to maintain their average size within steady state populations, but we do not yet have a full mechanistic understanding of how this is achieved (Chien et al, 2012). The cell size control strategy should be robust to different sources of noise such as variation in microenvironment, stochastic gene expression, and heterogeneity in cell physiology and growth. These strategies and their molecular mechanisms are beginning to be investigated in detail at the single cell level, Cell Size Control in Mycobacteria especially with model bacterial species such as Escherichia coil and Caulobacter crescentus (Campos et al, 2014; Taheri-Araghi et al, 2015) but how these principles apply to other bacterial systems such as mycobacteria is less well understood
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