EspJ effector in enterohemorrhagic E. coli translocates into host mitochondria via an atypical mitochondrial targeting signal
Article first published online: 8 MAR 2010
© 2010 The Societies and Blackwell Publishing Asia Pty Ltd
Microbiology and Immunology
Volume 54, Issue 7, pages 371–379, July 2010
How to Cite
Kurushima, J., Nagai, T., Nagamatsu, K. and Abe, A. (2010), EspJ effector in enterohemorrhagic E. coli translocates into host mitochondria via an atypical mitochondrial targeting signal. Microbiology and Immunology, 54: 371–379. doi: 10.1111/j.1348-0421.2010.00218.x
- Issue published online: 23 JUN 2010
- Article first published online: 8 MAR 2010
- Received 15 September 2009; revised 27 February 2010; accepted 1 March 2010.
- EspJ effector;
- enterohemorrhagic Escherichia coli;
- type III secretion system
EHEC is a bacterial pathogen causing diarrhea and hemorrhagic colitis in humans. To exert virulence, EHEC exploits a subset of effectors that are translocated into host cells via the type III secretion system. EspJ, which was recently identified as a type III secreted effector, is conserved in related pathogens such as EPEC and Citrobacter rodentium. However, the exact function of EspJ remains unclear. In the present study, we found that EspJ was unstable in host cells, which might be attributable to the N-terminal part beginning from amino acid number 59. Using stable forms of EspJ derivatives, we demonstrated for the first time that EspJ has the ability to translocate into mitochondria via an atypical mitochondrial targeting signal at the N terminus (1–36 a.a.) of EspJ. It has been reported that a mitochondrial targeting effector, EspF, disrupts the mitochondrial membrane potential, resulting in an induction of host cell death. To further investigate EspJ function in mitochondria, HeLa cells were infected with wild-type EPEC, an isogenic EspJ-mutant or an EspJ-overexpressing strain. The result of LDH release assay using an EspJ-mutant showed that the EspJ effector appears not to be involved in cytotoxicity.