Bacterial Nucleoid Occlusion: Multiple Mechanisms for Preventing Chromosome Bisection During Cell Division

In most bacteria cell division is driven by the prokaryotic tubulin homolog, FtsZ, which forms the cytokinetic Z ring. Cell survival demands both the spatial and temporal accuracy of this process to ensure that equal progeny are produced with intact genomes. While mechanisms preventing septum formation at the cell poles have been known for decades, the means by which the bacterial nucleoid is spared from bisection during cell division, called nucleoid exclusion (NO), have only recently been deduced. The NO theory was originally posited decades ago based on the key observation that the cell division machinery appeared to be inhibited from forming near the bacterial nucleoid. However, what might drive the NO process was unclear. Within the last 10 years specific proteins have been identified as important mediators of NO. Arguably the best studied NO mechanisms are those employed by the Escherichia coli SlmA and Bacillus subtilis Noc proteins. Both proteins bind specific DNA sequences within selected chromosomal regions to act as timing devices. However, Noc and SlmA contain completely different structural folds and utilize distinct NO mechanisms. Recent studies have identified additional processes and factors that participate in preventing nucleoid septation during cell division. These combined data show multiple levels of redundancy as well as a striking diversity of mechanisms have evolved to protect cells against catastrophic bisection of the nucleoid. Here we discuss these recent findings with particular emphasis on what is known about the molecular underpinnings of specific NO machinery and processes.