ArticleFEBS letters2005
Physiological stress of intracellular Shigella flexneri visualized with a metabolic sensor fused to a surface-reporter system.
Article in FEBS letters, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed, 1 citations in OpenAlex.
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5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When deleted of its N-terminal signal-reception domain, the broad host range sigma54-dependent transcriptional regulator XylR, along with its cognate promoter Pu, becomes a sensor of the metabolic stress of the carrier bacteria. We have employed a surface reporter system to visualize the physiological status of intracellular Shigella flexneri during infection of Henle 407 cells in culture. To this end, the xylRDeltaA gene has been engineered adjacent to a bicistronic transcriptional fusion of Pu to a lamB variant tagged with a short viral sequence (cor) and beta-galactosidase (lacZ). The accessibility of the cor epitope to the externalmost medium and the expression of Pu in the bacterial population was confirmed, respectively, with immunomagnetic beads and the sorting of Escherichia coli cells treated with a fluorescent antibody. Intracellular Shigella cells expressed the Pu-lamB/cor-lacZ reporter at high levels, suggesting that infectious cells endure a considerable metabolic constraint during the invasion process.
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