Enhancement of mitochondrial ATP production by the Escherichia coli cytotoxic necrotizing factor 1

Sara Travaglione, Stefano Loizzo, Teresa Rizza, Antonella Del Brocco, Giulia Ballan, Marco Guidotti, Rosa Vona, Michela Di Nottia, Alessandra Torraco, Rosalba Carrozzo, Carla Fiorentini, Alessia Fabbri

Research output: Contribution to journalArticle

Abstract

Mitochondria are dynamic organelles that constantly change shape and structure in response to different stimuli and metabolic demands of the cell. The Escherichia coli protein toxin cytotoxic necrotizing factor 1 (CNF1) has recently been reported to influence mitochondrial activity in a mouse model of Rett syndrome and to increase ATP content in the brain tissue of an Alzheimer's disease mouse model. In the present work, the ability of CNF1 to influence mitochondrial activity was investigated in IEC-6 normal intestinal crypt cells. In these cells, the toxin was able to induce an increase in cellular ATP content, probably due to an increment of the mitochondrial electron transport chain. In addition, the CNF1-induced Rho GTPase activity also caused changes in the mitochondrial architecture that mainly consisted in the formation of a complex network of elongated mitochondria. The involvement of the cAMP-dependent protein kinase A signaling pathway was postulated. Our results demonstrate that CNF1 positively affects mitochondria by bursting their energetic function and modifying their morphology.

Original languageEnglish
Pages (from-to)3473-3488
Number of pages16
JournalFEBS Journal
Volume281
Issue number15
DOIs
Publication statusPublished - 2014

Keywords

  • ATP
  • CNF1
  • Drp1
  • mitochondria
  • PKA

ASJC Scopus subject areas

  • Biochemistry
  • Cell Biology
  • Molecular Biology

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    Travaglione, S., Loizzo, S., Rizza, T., Del Brocco, A., Ballan, G., Guidotti, M., Vona, R., Di Nottia, M., Torraco, A., Carrozzo, R., Fiorentini, C., & Fabbri, A. (2014). Enhancement of mitochondrial ATP production by the Escherichia coli cytotoxic necrotizing factor 1. FEBS Journal, 281(15), 3473-3488. https://doi.org/10.1111/febs.12874