Journal article
Substrate recognition by the zinc metalloprotease effector NleC from enteropathogenic Escherichia coli
C Giogha, T Wong Fok Lung, S Mühlen, JS Pearson, EL Hartland
Cellular Microbiology | WILEY-BLACKWELL | Published : 2015
DOI: 10.1111/cmi.12469
Abstract
Upon infection of epithelial cells, enteropathogenic Escherichiacoli suppresses host cell inflammatory signalling in a type III secretion system (T3SS) dependent manner. Two key T3SS effector proteins involved in this response are NleE and NleC. NleC is a zinc metalloprotease effector that degrades the p65 subunit of NF-κB. Although the site of p65 cleavage by NleC is now well described, other areas of interaction have not been precisely defined. Here we constructed overlapping truncations of p65 to identify regions required for NleC cleavage. We determined that NleC cleaved both p65 and p50 within the Rel homology domain (RHD) and that two motifs, E22IIE25 and P177VLS180, within the RHD of ..
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Awarded by Australian National Health and Medical Research Council
Funding Acknowledgements
We are indebted to Neil Perkins (University of Newcastle, UK) for the gift of pBluescript-p50 and Michael White (Centre for Cell Imaging, University of Liverpool, UK) for the gift of pGFP-p65. This work was supported by grants to ELH from the Australian National Health and Medical Research Council (APP606788). CG is the recipient of an Australian Postgraduate Award. TW is the recipient of a University of Melbourne International Research Scholarship.