Please use this identifier to cite or link to this item: https://doi.org/10.1371/journal.pone.0001291
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dc.titleModulation of bacterial type III secretion system by a spermidine transporter dependent signaling pathway
dc.contributor.authorZhou, L.
dc.contributor.authorWang, J.
dc.contributor.authorZhang, L.-H.
dc.date.accessioned2014-10-27T08:33:41Z
dc.date.available2014-10-27T08:33:41Z
dc.date.issued2007-12-12
dc.identifier.citationZhou, L., Wang, J., Zhang, L.-H. (2007-12-12). Modulation of bacterial type III secretion system by a spermidine transporter dependent signaling pathway. PLoS ONE 2 (12) : -. ScholarBank@NUS Repository. https://doi.org/10.1371/journal.pone.0001291
dc.identifier.issn19326203
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/101113
dc.description.abstractBackground. Many gram-negative bacterial pathogens employ Type III secretion systems (T3SS) to inject effector proteins into host cells in infectious processes. Methodology/Principal Findings. By screening a transposon mutant library of P. aeruginosa, we found that mutation of spuDEFGH, which encode a major spermidine uptake system, abolished the expression of the exsCEBA operon that codes for key T3SS regulators under inducing conditions (low calcium). Whole genome microarray analysis revealed that inactivation of the spermidine uptake system significantly decreased the transcriptional expression of most, if not all, T3SS genes. Consistently, the spermidine uptake mutants showed decreased expression of the T3SS genes in responding to host cell extract and attenuated cytotoxicity. Furthermore, exogenous addition of spermidine to the wild type strain PAO1 enhanced the expression of exsCEBA and also the effector protein genes. Conclusion/Significance. Cumulatively, these data have depicted a novel spermidine transporter-dependent signaling pathway, which appears to play an essential role in modulation of T3SS expression in P. aeruginosa. © 2007 Zhou et al.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1371/journal.pone.0001291
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentBIOLOGICAL SCIENCES
dc.description.doi10.1371/journal.pone.0001291
dc.description.sourcetitlePLoS ONE
dc.description.volume2
dc.description.issue12
dc.description.page-
dc.identifier.isiut000207459500010
dc.published.statePublished
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