<i>Chlamydia</i> preserves the mitochondrial network necessary for replication via microRNA-dependent inhibition of fission

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  • Suvagata Roy Chowdhury
    Department of Microbiology, Biocenter, University of Würzburg, 97074 Würzburg, Germany 1
  • Anastasija Reimer
    Department of Microbiology, Biocenter, University of Würzburg, 97074 Würzburg, Germany 1
  • Malvika Sharan
    Institute for Molecular Infection Biology, University of Würzburg, 97080 Würzburg, Germany 2
  • Vera Kozjak-Pavlovic
    Department of Microbiology, Biocenter, University of Würzburg, 97074 Würzburg, Germany 1
  • Ana Eulalio
    Institute for Molecular Infection Biology, University of Würzburg, 97080 Würzburg, Germany 2
  • Bhupesh K. Prusty
    Department of Microbiology, Biocenter, University of Würzburg, 97074 Würzburg, Germany 1
  • Martin Fraunholz
    Department of Microbiology, Biocenter, University of Würzburg, 97074 Würzburg, Germany 1
  • Karthika Karunakaran
    Department of Microbiology, Biocenter, University of Würzburg, 97074 Würzburg, Germany 1
  • Thomas Rudel
    Department of Microbiology, Biocenter, University of Würzburg, 97074 Würzburg, Germany 1

説明

<jats:p>Obligate intracellular bacteria such as Chlamydia trachomatis depend on metabolites of the host cell and thus protect their sole replication niche by interfering with the host cells’ stress response. Here, we investigated the involvement of host microRNAs (miRNAs) in maintaining the viability of C. trachomatis–infected primary human cells. We identified miR-30c-5p as a prominently up-regulated miRNA required for the stable down-regulation of p53, a major suppressor of metabolite supply in C. trachomatis–infected cells. Loss of miR-30c-5p led to the up-regulation of Drp1, a mitochondrial fission regulator and a target gene of p53, which, in turn, severely affected chlamydial growth and had a marked effect on the mitochondrial network. Drp1-induced mitochondrial fragmentation prevented replication of C. trachomatis even in p53-deficient cells. Additionally, Chlamydia maintain mitochondrial integrity during reactive oxygen species–induced stress that occurs naturally during infection. We show that C. trachomatis require mitochondrial ATP for normal development and hence postulate that they preserve mitochondrial integrity through a miR-30c-5p–dependent inhibition of Drp1-mediated mitochondrial fission.</jats:p>

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