Abstract

Bacteria are simpler than eukaryotic cells, and have served for decades as model systems to investigate various levels of biological questions. They are also of course immensely important physiologically and technologically. In this scenario E.Coli has been a model organism – and yet it is still not clear how a variety of very simple processes are carried out by these cells.

Many of these open questions are not to do with specific molecular mechanisms, but are instead one level “up” in complexity. Examples go from how the chromosomes partition robustly into opposite sides of the cell, ready for division, to how the physical conformation of the chromosome at various scales affects gene expression, and to how rod-like bacteria like E.Coli “know” when to initiate cell division. At this level, the questions have as much to do with physics as they have with the underlying specific molecular mechanisms.

We will focus on just one aspect on which we have been active recently, working experimentally in our lab, and developing theory particularly with M.Cosentino Lagomarsino in Paris. I will describe efforts at disentangling the source of size control in E.Coli. Working not at the level of molecular mechanisms, but looking instead at a large dataset of single cell growth rate and cell size at division, we conclude that E.Coli cell size is not regulated by neither a pure “sizer” nor “timer”, and we caution against thinking the topic is settled with the recently proposed “adder” mechanism.