Abstract
An immediately observable feature of bacteria is that cell size and shape are remarkably constant and characteristic for a given species in a particular condition, but vary quantitatively with physiological parameters such as growth rate, indicating both genetic and environmental regulation. However, despite decades of research, the molecular mechanisms underlying bacterial morphogenesis have remained incompletely characterized. We recently demonstrated that a wide range of bacterial species exhibit a robust surface area to volume ratio (SA/V) homeostasis. Because cell size, shape, and SA/V are mathematically interconnected, if SA/V is indeed the natural variable that cells actively monitor, this finding has critical implications for our understanding of bacterial morphogenesis, placing fundamental constraints on the sizes and shapes that cells can adopt. In this Opinion article we discuss the broad implications that this novel perspective has for the field of bacterial growth and morphogenesis.
Highlights
An immediately observable feature of bacteria is that cell size and shape are remarkably constant and characteristic for a given species in a particular condition, but vary quantitatively with physiological parameters such as growth rate, indicating both genetic and environmental regulation
surface area to volume ratio (SA/V) homeostasis arises because the rate of surface growth scales with cell volume, and evidence suggests that this scaling is likely due to the biosynthesis of new peptidoglycan (PG) in the cytoplasm setting the rate of surface growth
Given the predictive power of this model, we propose that SA/V is the critical natural variable to consider when looking at bacterial morphogenesis
Summary
Revealed that cells move toward a new steady-state SA/V in this manner, providing strong, quantitative support for this mechanism of SA/V homeostasis [13]. When diverse bacterial species were treated with very low doses of the antibiotic fosfomycin, which inhibits the first committed step of PG biosynthesis, cells continued growing their volume essentially uninterrupted (i.e., a did not change), but slowed down the rate of surface growth per unit volume (i.e., b was reduced) [13] This implies that the scaling between volume and surface growth, at least in this regime, is determined by the flux through the PG biosynthesis pathway. Disruption of late steps in the O-antigen and ECA biosynthesis pathways leads to a buildup of Und-P-linked dead end intermediates, which sequester Und-P away from PG biosynthesis [23,24] The authors of these studies demonstrated that the observed increases in cell size are due to reduced production of PG, not the other envelope constituents, further supporting the proposal that PG biosynthesis provides the main molecular link between cell volume and surface growth in the ‘relative rates’ model.
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