Functional high-throughput screening identifies the miR-15 microRNA family as cellular restriction factors for Salmonella infection

Claire Maudet, Miguel Mano, Ushasree Sunkavalli, Malvika Sharan, Mauro Giacca, Konrad U. Förstner and Ana Eulalio ()
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Claire Maudet: Institute for Molecular Infection Biology (IMIB), University of Würzburg, Josef-Schneider-Strasse 2/D15
Miguel Mano: International Centre for Genetic Engineering and Biotechnology (ICGEB), Padriciano 99
Ushasree Sunkavalli: Institute for Molecular Infection Biology (IMIB), University of Würzburg, Josef-Schneider-Strasse 2/D15
Malvika Sharan: Institute for Molecular Infection Biology (IMIB), University of Würzburg, Josef-Schneider-Strasse 2/D15
Mauro Giacca: International Centre for Genetic Engineering and Biotechnology (ICGEB), Padriciano 99
Konrad U. Förstner: Institute for Molecular Infection Biology (IMIB), University of Würzburg, Josef-Schneider-Strasse 2/D15
Ana Eulalio: Institute for Molecular Infection Biology (IMIB), University of Würzburg, Josef-Schneider-Strasse 2/D15

Nature Communications, 2014, vol. 5, issue 1, 1-13

Abstract: Abstract Increasing evidence suggests an important role for miRNAs in the molecular interplay between bacterial pathogens and host cells. Here we perform a fluorescence microscopy-based screen using a library of miRNA mimics and demonstrate that miRNAs modulate Salmonella infection. Several members of the miR-15 miRNA family were among the 17 miRNAs that more efficiently inhibit Salmonella infection. We discovered that these miRNAs are downregulated during Salmonella infection, through the inhibition of the transcription factor E2F1. Analysis of miR-15 family targets revealed that derepression of cyclin D1 and the consequent promotion of G1/S transition are crucial for Salmonella intracellular proliferation. In addition, Salmonella induces G2/M cell cycle arrest in infected cells, further promoting its replication. Overall, these findings uncover a mechanism whereby Salmonella renders host cells more susceptible to infection by controlling cell cycle progression through the active modulation of host cell miRNAs.

Date: 2014
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DOI: 10.1038/ncomms5718

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