# Bacterial chromatin remodeling associated with transcription-induced domains at pathogenicity Islands

**Authors:** Mounia Kortebi, Mickaël Bourge, Romain Le Bars, Erwin Van Dijk, Charles J. Dorman, Stéphanie Bury-Moné, Frédéric Boccard, Virginia S. Lioy

PMC · DOI: 10.1038/s41467-025-67746-w · Nature Communications · 2026-01-08

## TL;DR

This study shows how Salmonella bacteria regulate harmful genes by restructuring their DNA and positioning them near the cell's edge when they become active.

## Contribution

The study reveals how chromatin remodeling and spatial repositioning regulate SPI-1 gene expression in Salmonella.

## Key findings

- Silent SPIs are linked to antisense transcription from H-NS-free regions.
- SPI-1 activation causes H-NS remodeling and forms transcription-induced domains.
- SPI-1 repositions to the nucleoid periphery when activated.

## Abstract

The nucleoid-associated protein H-NS is a bacterial xenogeneic silencer responsible for preventing costly expression of genes acquired through horizontal gene transfer. H-NS silences several Salmonella Pathogenicity Islands (SPIs) essential for host infection. The stochastic expression of SPI-1 is required for invasion of host epithelial cells but complicates investigation of factors involved in SPI-1 chromatin structure and regulation. We performed functional genomics on sorted Salmonella populations expressing SPI-1 or not, to characterize how SPI-1 activation affects chromatin composition, DNA conformation, gene expression and SPI-1 subcellular localization. We show that silent SPIs are associated with spurious antisense transcriptional activity originating from H-NS-free regions. Upon SPI-1 activation, remodeling of H-NS occupancy defines a new chromatin landscape, which together with the master SPI-1 regulator HilD, facilitates transcription of SPI-1 genes. SPI-1 activation promotes formation of Transcription Induced Domains accompanied by repositioning SPI-1 close to the nucleoid periphery. We present a model for tightly regulated chromatin remodeling that minimizes the cost of pathogenicity island activation.

The bacterial protein H-NS prevents costly expression of horizontally acquired genes such as those in Salmonella pathogenicity islands (SPIs), which are essential for infection. Here, Kortebi et al. show that the expression of SPI-1 is associated with Salmonella chromatin remodelling and with the repositioning of this region toward the nucleoid periphery.

## Linked entities

- **Genes:** SPI1 (Spi-1 proto-oncogene) [NCBI Gene 6688], hns (histone-like protein Hns) [NCBI Gene 886187], hilD (regulatory helix-turn-helix proteins, araC family) [NCBI Gene 1254398]
- **Proteins:** hns (histone-like protein Hns), hilD (regulatory helix-turn-helix proteins, araC family)
- **Species:** Salmonella (taxon 590)

## Full-text entities

- **Genes:** SPI1 (Spi-1 proto-oncogene) [NCBI Gene 6688] {aka AGM10, OF, PU.1, SFPI1, SPI-1, SPI-A}
- **Diseases:** infection (MESH:D007239)
- **Species:** Salmonella (genus) [taxon 590]

## Full text

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## Figures

6 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12783615/full.md

## References

11 references — full list in the complete paper: https://tomesphere.com/paper/PMC12783615/full.md

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Source: https://tomesphere.com/paper/PMC12783615