Journal
CELLULAR MICROBIOLOGY
Volume 13, Issue 10, Pages 1542-1557Publisher
WILEY
DOI: 10.1111/j.1462-5822.2011.01640.x
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Funding
- National Sciences and Engineering Research Council of Canada (NSERC)
- Canadian Institute of Health Research (CIHR)
- Michael Smith Foundation for Health Research (MSFHR)
- Canadian Association of Gastroenterology (CAG)
- Ferring Pharmaceuticals
- HHMI
- Infectious Diseases and Parasitology
- Genome Canada/Genome British Columbia
- Canada Foundation for Innovation
- British Columbia (BC) through the BC Proteomics Network (BCPN)
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Enteropathogenic and enterohaemorrhagic Escherichia coli (EPEC and EHEC respectively) are attaching and effacing bacterial pathogens that cause devastating diarrhoeal disease worldwide. These pathogens depend on a type III secretion system, which functions as a molecular syringe to translocate bacterial effector proteins directly into infected host cells. One of these effectors, NleC, was recently described as a zinc metalloprotease that targets NF-kappa B Rel-A (p65) and thus contributes to dampening of inflammatory signalling during EPEC and EHEC infection. We have identified the acetyltransferase p300 as an additional target of NleC. Several biochemical techniques were employed to demonstrate specific binding of p300 by NleC. We also show that NleC causes decreased abundance of p300 in cellular nuclei and that the metalloprotease domain of NleC is responsible for this phenotype. Furthermore, we demonstrate that overexpression of p300 can antagonize repression of IL-8 secretion by EPEC and that siRNA knockdown of p300 dampens IL-8 secretion by EPEC Delta nleC-infected cells. We have therefore identified a second target of NleC and provided the first example of a bacterial virulence factor targeting the acetyltransferase p300.
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