Bacterial cell shape is a key trait governing the extracellular and intracellular factors of bacterial life. Rod-like cell shape appears to be original which implies that the cell wall, division, and rod-like shape came together in ancient bacteria and that the myriad of shapes observed in extant bacteria have evolved from this ancestral shape. In order to understand its evolution, we must first understand how this trait is actively maintained through the construction and maintenance of the peptidoglycan cell wall. The proteins that are primarily responsible for cell shape are therefore the elements of the bacterial cytoskeleton, principally FtsZ, MreB, and the penicillin-binding proteins. MreB is particularly relevant in the transition between rod-like and spherical cell shape as it is often (but not always) lost early in the process. Here we will highlight what is known of this particular transition in cell shape and how it affects fitness before giving a brief perspective on what will be required in order to progress the field of cell shape evolution from a purely mechanistic discipline to one that has the perspective to both propose and to test reasonable hypotheses regarding the ecological drivers of cell shape change.

Cell shape is a fundamental property in bacterial kingdom. MreB is a protein 22 that determines rod-like shape, and its deletion is generally lethal. Here, we 23 deleted the mreB homolog from rod-shaped bacterium Pseudomonas fluorescens 24 SBW25 and found that ΔmreB cells are viable, spherical cells with a 20% 25 reduction in competitive fitness and high variability in cell size. We show that 26 cell death, correlated with increased levels of elongation asymmetry between 27 sister cells, accounts for the large fitness reduction. After a thousand generations 28 in rich media, the fitness of evolved ΔmreB lines was restored to ancestral levels 29 and cells regained symmetry and ancestral size, while maintaining spherical 30 shape. Using population sequencing, we identified pbp1A, coding for a protein 31 involved in cell wall synthesis, as the primary target for compensatory mutations 32 of the ΔmreB genotype. Our findings suggest that reducing elongasome 33 associated PBPs aids in the production of symmetric cells when MreB is absent. 34 35