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Investigating the effect of bacteriophages on bacterial FtsZ localisation

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Dhaonoa, Gurneet K., Kushnir, Inbar, Qimron, Udi, Roper, David I. and Sagona, Antonia P. (2022) Investigating the effect of bacteriophages on bacterial FtsZ localisation. Frontiers in Cellular and Infection Microbiology-Microbiome in Health and Disease, 12 . 863712. doi:10.3389/fcimb.2022.863712 ISSN 2235-2988.

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Official URL: https://doi.org/10.3389/fcimb.2022.863712

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Abstract

Escherichia coli is one of the most common Gram-negative pathogens and is responsible for infection leading to neonatal meningitis and sepsis. The FtsZ protein is a bacterial tubulin homolog required for cell division in most species, including E. coli. Several agents that block cell division have been shown to mislocalise FtsZ, including the bacteriophage -encoded Kil peptide, resulting in defective cell division and a filamentous phenotype, making FtsZ an attractive target for antimicrobials. In this study we have used an in vitro meningitis model system for studying the effect of bacteriophages on FtsZ using fluorescent E. coli EV36/FtsZ-mCherry and K12/FtsZ-mNeon strains. We show localisation of FtsZ to the bacterial cell midbody as a single ring during normal growth conditions, and mislocalisation of FtsZ producing filamentous multi-ringed bacterial cells upon addition of the known inhibitor Kil peptide. We also show that when bacteriophages K1F-GFP and T7-mCherry were applied to their respective host strains, these phages can inhibit FtsZ and block bacterial cell division leading to a filamentous multi-ringed phenotype, potentially delaying lysis and increasing progeny number. This occurs in the exponential growth phase, as actively dividing hosts are needed. We present that the ZapA protein is needed for phage inhibition by showing a phenotype recovery with a ZapA mutant strain, and we show that the FtsI protein is also mislocalised upon phage infection. Finally, we show that the T7 peptide gp0.4 is responsible for inhibition of FtsZ in K12 strains by observing a phenotype recovery with a T7∆0.4 mutant.

Item Type: Journal Article
Subjects: Q Science > QH Natural history
Q Science > QP Physiology
Q Science > QR Microbiology
Divisions: Faculty of Science, Engineering and Medicine > Science > Life Sciences (2010- )
Library of Congress Subject Headings (LCSH): Bacteriophages, Cell division, Tubulins , Drug resistance in microorganisms
Journal or Publication Title: Frontiers in Cellular and Infection Microbiology-Microbiome in Health and Disease
Publisher: Frontiers
ISSN: 2235-2988
Official Date: 29 July 2022
Dates:
DateEvent
29 July 2022Published
4 July 2022Accepted
Volume: 12
Article Number: 863712
DOI: 10.3389/fcimb.2022.863712
Status: Peer Reviewed
Publication Status: Published
Access rights to Published version: Open Access (Creative Commons)
Date of first compliant deposit: 4 July 2022
Date of first compliant Open Access: 4 July 2022
RIOXX Funder/Project Grant:
Project/Grant IDRIOXX Funder NameFunder ID
BB/N011872/1[BBSRC] Biotechnology and Biological Sciences Research Councilhttp://dx.doi.org/10.13039/501100000268
Midlands Integrative Biosciences Training PartnershipUniversity of Warwickhttp://dx.doi.org/10.13039/501100000741
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