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Enhancement of mitochondrial ATP production by the Escherichia coli cytotoxic necrotizing factor 1
Author(s) -
Travaglione Sara,
Loizzo Stefano,
Rizza Teresa,
Del Brocco Antonella,
Ballan Giulia,
Guidotti Marco,
Vona Rosa,
Di Nottia Michela,
Torraco Alessandra,
Carrozzo Rosalba,
Fiorentini Carla,
Fabbri Alessia
Publication year - 2014
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.12874
Subject(s) - mitochondrion , microbiology and biotechnology , cytotoxic t cell , biology , bioenergetics , organelle , gtpase , escherichia coli , electron transport chain , biochemistry , chemistry , gene , in vitro
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 ( CNF 1) 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 CNF 1 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 CNF 1‐induced Rho GTP ase 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 c AMP ‐dependent protein kinase A signaling pathway was postulated. Our results demonstrate that CNF 1 positively affects mitochondria by bursting their energetic function and modifying their morphology.