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Mutations Affecting HVO_1357 or HVO_2248 Cause Hypermotility in Haloferax volcanii, Suggesting Roles in Motility Regulation

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Dyall-Smith,  Mike
Habermann, Bianca / Computational Biology, Max Planck Institute of Biochemistry, Max Planck Society;

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Pfeiffer,  Friedhelm
Habermann, Bianca / Computational Biology, Max Planck Institute of Biochemistry, Max Planck Society;

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genes-12-00058-v3.pdf
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genes-12-00058-s001.zip
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Citation

Collins, M., Afolayan, S., Igiraneza, A. B., Schiller, H., Krespan, E., Beiting, D. P., et al. (2021). Mutations Affecting HVO_1357 or HVO_2248 Cause Hypermotility in Haloferax volcanii, Suggesting Roles in Motility Regulation. Genes, 12(1): 58. doi:10.3390/genes12010058.


Cite as: https://hdl.handle.net/21.11116/0000-0008-1291-F
Abstract
Motility regulation plays a key role in prokaryotic responses to environmental stimuli. Here, we used a motility screen and selection to isolate hypermotile Haloferax volcanii mutants from a transposon insertion library. Whole genome sequencing revealed that hypermotile mutants were predominantly affected in two genes that encode HVO_1357 and HVO_2248. Alterations of these genes comprised not only transposon insertions but also secondary genome alterations. HVO_1357 contains a domain that was previously identified in the regulation of bacteriorhodopsin transcription, as well as other domains frequently found in two-component regulatory systems. The genes adjacent to hvo_1357 encode a sensor box histidine kinase and a response regulator, key players of a two-component regulatory system. None of the homologues of HVO_2248 have been characterized, nor does it contain any of the assigned InterPro domains. However, in a significant number of Haloferax species, the adjacent gene codes for a chemotaxis receptor/transducer. Our results provide a foundation for characterizing the root causes underlying Hfx. volcanii hypermotility.