H-NS is a bacterial transposon capture protein

The histone-like nucleoid structuring (H-NS) protein is a DNA binding factor, found in gammaproteobacteria, with functional equivalents in diverse microbes. Universally, such proteins are understood to silence transcription of horizontally acquired genes. Here, we identify transposon capture as a major overlooked function of H-NS. Using genome-scale approaches, we show that H-NS bound regions are transposition "hotspots". Since H-NS often interacts with pathogenicity islands, such targeting creates clinically relevant phenotypic diversity. For example, in Acinetobacter baumannii, we identify altered motility, biofilm formation, and interactions with the human immune system. Transposon capture is mediated by the DNA bridging activity of H-NS and, if absent, more ubiquitous transposition results. Consequently, transcribed and essential genes are disrupted. Hence, H-NS directs transposition to favour evolutionary outcomes useful for the host cell.

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Publication Details

Journal
Nature Communications
Published
2024-08-20
DOI
https://doi.org/10.1038/s41467-024-51407-5
Citations
26
Primary Topic
Antibiotic Resistance in Bacteria
Type
article
Field-Weighted Citation Impact
4.43

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article

H-NS is a bacterial transposon capture protein

David C. Grainger, David Forrest, Rachel Wheat, Charles Cooper et al.
26 citations
Nature Communications
Antibiotic Resistance in Bacteria
4.43
article

H-NS is a bacterial transposon capture protein

David C. Grainger, David Forrest, Rachel Wheat, Charles Cooper, Prateek Sharma, Simon Legood, James R. J. Haycocks
article en
26 citations

Abstract

The histone-like nucleoid structuring (H-NS) protein is a DNA binding factor, found in gammaproteobacteria, with functional equivalents in diverse microbes. Universally, such proteins are understood to silence transcription of horizontally acquired genes. Here, we identify transposon capture as a major overlooked function of H-NS. Using genome-scale approaches, we show that H-NS bound regions are transposition "hotspots". Since H-NS often interacts with pathogenicity islands, such targeting creates clinically relevant phenotypic diversity. For example, in Acinetobacter baumannii, we identify altered motility, biofilm formation, and interactions with the human immune system. Transposon capture is mediated by the DNA bridging activity of H-NS and, if absent, more ubiquitous transposition results. Consequently, transcribed and essential genes are disrupted. Hence, H-NS directs transposition to favour evolutionary outcomes useful for the host cell.

Nature CommunicationsVol. 15(1)
University of Birmingham (GB)
Wellcome, Wellcome Trust
Life below water
Openalex Percentile: Top 4%
Antibiotic Resistance in Bacteria
4.43
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