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. 2007 Sep 13;2(3):160-71.
doi: 10.1016/j.chom.2007.07.010.

The bacterial virulence factor NleA inhibits cellular protein secretion by disrupting mammalian COPII function

Jinoh Kim  1 , Ajitha Thanabalasuriar, Tessa Chaworth-Musters, J Chris Fromme, Elizabeth A Frey, Paula I Lario, Pavel Metalnikov, Keyrillos Rizg, Nikhil A Thomas, Sau Fung Lee, Elizabeth L Hartland, Philip R Hardwidge, Tony Pawson, Natalie C Strynadka, B Brett Finlay, Randy Schekman, Samantha Gruenheid
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Free article

The bacterial virulence factor NleA inhibits cellular protein secretion by disrupting mammalian COPII function

Jinoh Kim et al. Cell Host Microbe. .
Free article

Abstract

Enterohemorrhagic and enteropathogenic Escherichia coli (EHEC and EPEC) maintain an extracellular lifestyle and use a type III secretion system to translocate effector proteins into the host cytosol. These effectors manipulate host pathways to favor bacterial replication and survival. NleA is an EHEC/EPEC- and related species-specific translocated effector protein that is essential for bacterial virulence. However, the mechanism by which NleA impacts virulence remains undetermined. Here we demonstrate that NleA compromises the Sec23/24 complex, a component of the mammalian COPII protein coat that shapes intracellular protein transport vesicles, by directly binding Sec24. Expression of an NleA-GFP fusion protein reduces the efficiency of cellular secretion by 50%, and secretion is inhibited in EPEC-infected cells. Direct biochemical experiments show that NleA inhibits COPII-dependent protein export from the endoplasmic reticulum. Collectively, these findings indicate that disruption of COPII function in host cells contributes to the virulence of EPEC and EHEC.

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