In stable environments, cell size fluctuations are thought to be governed by simple physical principles, as suggested by recent findings of scaling properties. Here, by developing a microfluidic device and using E. coli, we investigate the response of cell size fluctuations against starvation. By abruptly switching to non-nutritious medium, we find that the cell size distribution changes but satisfies scale invariance: the rescaled distribution is kept unchanged and determined by the growth condition before starvation. These findings are underpinned by a model based on cell growth and cell cycle. Further, we numerically determine the range of validity of the scale invariance over various characteristic times of the starvation process, and find the violation of the scale invariance for slow starvation. Our results, combined with theoretical arguments, suggest the relevance of the multifork replication, which helps retaining information of cell cycle states and may thus result in the scale invariance.

We study competition of two non-motile bacterial strains in a three-dimensional channel numerically, and analyze how their configuration evolves in space and time. We construct a lattice model that takes into account self-replication, mutation, and killing of bacteria. When mutation is not significant, the two strains segregate and form stripe patterns along the channel. The formed lanes are gradually rearranged, with increasing length scales in the two-dimensional cross-sectional plane. We characterize it in terms of coarsening and phase ordering in statistical physics. In particular, for the simple model without mutation and killing, we find logarithmically slow coarsening, which is characteristic of the two-dimensional voter model. With mutation and killing, we find a phase transition from a monopolistic phase, in which lanes are formed and coarsened until the system is eventually dominated by one of the two strains, to an equally mixed and disordered phase without lane structure. Critical behavior at the transition point is also studied and compared with the generalized voter class and the Ising class. These results are accounted for by continuum equations, obtained by applying a mean field approximation along the channel axis. Our findings indicate relevance of critical coarsening of two-dimensional systems in the problem of bacterial competition within anisotropic three-dimensional geometry.arXiv:1804.09895v3 [q-bio.PE]

Rod-shaped bacteria, such as Escherichia coli, commonly live forming mounded colonies. They initially grow two-dimensionally on a surface and finally achieve three-dimensional growth. While it was recently reported that three-dimensional growth is promoted by topological defects of winding number +1/2 in populations of motile bacteria, how cellular alignment plays a role in nonmotile cases is largely unknown. Here, we investigate the relevance of topological defects in colony formation processes of nonmotile E. coli populations, and found that both ±1/2 topological defects contribute to the three-dimensional growth. Analyzing the cell flow in the bottom layer of the colony, we observe that +1/2 defects attract cells and −1/2 defects repel cells, in agreement with previous studies on motile cells, in the initial stage of the colony growth. However, later, cells gradually flow toward −1/2 defects as well, exhibiting a sharp contrast to the existing knowledge. By investigating three-dimensional cell orientations by confocal microscopy, we find that vertical tilting of cells is promoted near the defects. Crucially, this leads to the emergence of a polar order in the otherwise nematic two-dimensional cell orientation. We extend the theory of active nematics by incorporating this polar order and the vertical tilting, which successfully explains the influx toward −1/2 defects in terms of a polarity-induced force. Our work reveals that three-dimensional cell orientations may result in qualitative changes in properties of active nematics, especially those of topological defects, which may be generically relevant in active matter systems driven by cellular growth instead of self-propulsion.