Imperial College London
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ProfessorJ SimonKroll

Faculty of Medicine, Department of Infectious Disease

Emeritus Professor,Paediatrics&Molecular Infectious Diseases
 
 
 
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Contact

 

+44 (0)20 7594 3695s.kroll

 
 
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Assistant

 

Dr Robert Boyle +44 (0)20 7594 3990

 
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Location

 

245Wright Fleming WingSt Mary's Campus

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Summary

 

Publications

Citation

BibTex format

@article{Kroll:2017:10.1128/IAI.00574-16,
author = {Kroll, J and Li, M-S and langford, P},
doi = {10.1128/IAI.00574-16},
journal = {Infection and Immunity},
title = {Inactivation of NMB0419 encoding a Sel1-like repeat (SLR) protein in Neisseria meningitidis is associated with differential expression of genes belonging to the Fur regulon and reduced intra-epithelial replication},
url = {http://dx.doi.org/10.1128/IAI.00574-16},
volume = {85},
year = {2017}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Neisseria meningitidis is a commensal microbe that colonizes the human nasopharynx but occasionally invades the bloodstream to cause life-threatening infection. N. meningitidis MC58 NMB0419 encodes a Sel1-like repeat (SLR)-containing protein, previously implicated in invasion of epithelial cells. A gene-regulatory function was revealed in Escherichia coli expressing plasmid-borne NMB0419 showing significantly increased epithelial adherence compared to wild type, due to increased expression of mannose-sensitive type 1 pili. While a meningococcal NMB0419 mutant did not have altered epithelial adherence, in a transcriptome-wide comparison of wild type and an NMB0419 mutant, a large proportion of genes differentially regulated in the mutant were involved in iron acquisition and metabolism. Fifty one and 38% of genes respectively up- and down-regulated in the NMB0419 mutant had previously been identified as being induced and repressed by meningococcal Fur.  An in vitro growth defect of the NMB0419 mutant under iron-restriction was consistent with the down-regulation of tbpAB and hmbR, while an intra-epithelial replication defect was consistent with the down-regulation of tonB, exbB and exbD, based on a known phenotype of a meningococcal tonB mutant. Disruption of the N-terminal NMB0419 signal peptide, predicted to export the protein beyond the cytoplasmic membrane, resulted in loss of functional traits in N. meningitidis and E. coli. Our study indicates that the expression of NMB0419 is associated with transcriptional changes counterbalancing the regulatory function of Fur, offering a new perspective on regulatory mechanisms involved in meningococcal interaction with epithelial cells, and suggests new insights into the roles of SLR-containing genes in other bacteria.
AU  - Kroll,J
AU  - Li,M-S
AU  - langford,P
DO  - 10.1128/IAI.00574-16
PY  - 2017///
SN  - 1098-5522
TI  - Inactivation of NMB0419 encoding a Sel1-like repeat (SLR) protein in Neisseria meningitidis is associated with differential expression of genes belonging to the Fur regulon and reduced intra-epithelial replication
T2  - Infection and Immunity
UR  - http://dx.doi.org/10.1128/IAI.00574-16
UR  - http://hdl.handle.net/10044/1/45102
VL  - 85
ER  -
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