changes. Since MukB and HU have emerged as critical players in long-range DNA interactions, it will be worthwhile to compare the effect of each of these two proteins on global gene expression. Although HU appears to control gene expression by modulating supercoiling density, the exact molecular mechanism remains unknown and the impact of MukB on gene expression is yet to be analyzed. Spatial organization Chromosomal interaction domains In recent years, the advent of a molecular method called chromosome conformation capture (3C) has allowed studying a high-resolution spatial organization of chromosomes in both bacteria and eukaryotes. 3C and its version that is coupled with deep sequencing (Hi-C) determine physical proximity, if any, between any two genomic loci in 3D space. A high-resolution contact map of bacterial chromosomes including the E. coli chromosome has revealed that a bacterial chromosome is segmented into many highly self-interacting regions called chromosomal interaction domains (CIDs). CIDs are equivalent to topologically associating domains (TADs) observed in many eukaryotic chromosomes, suggesting that the formation of CIDs is a general phenomenon of genome organization. Two characteristics define CIDs or TADs. First, genomic regions of a CID physically interact with each other more frequently than with the genomic regions outside that CID or with those of a neighboring CID. Second, the presence of a boundary between CIDs that prevents physical interactions between genomic regions of two neighboring CIDs. The E. coli chromosome was found to consist of 31 CIDs in the growth phase. The size of the CIDs ranged from 40 to ~300 kb. It appears that a supercoiling-diffusion barrier responsible for segregating plectonemic DNA loops into topological domains functions as a CID boundary in E. coli and many other bacteria. In other words, the presence of a supercoiling-diffusion barrier defines the formation of CIDs. Findings from the Hi-C probing of chromosomes in E. coli, Caulobacter crescentus, and Bacillus subtilis converge on a model that CIDs form because plectonemic looping together with DNA organization activities of NAPs promotes physical interactions among genomic loci, and a CID boundary consists of a plectoneme-free region (PFR) that prevents these interactions. A PFR is created due to high transcription activity because the helical unwinding of DNA by actively transcribing RNAP restrains plectonemic supercoils. As a result, dissipation of supercoils is also blocked, creating a supercoiling-diffusion barrier. Indirect evidence for this model comes from an observation that CIDs of bacterial chromosomes including the E. coli