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Enterohemorrhagic E. coli effector NleL disrupts host NF-κB signaling by targeting multiple host proteins
Xiangpeng Sheng1,2,7,† , Qing You1,2,† , Hongnian Zhu3,† , Qingrun Li1 , Hong Gao4 , Haifeng Wang1 , Chunping You5 , Qing Meng3 , Yingjie Nie6 , Xiangyan Zhang6,* , Ronggui Hu1,*
1State Key Laboratory of Molecular Biology, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences, Shanghai 200031, China
2University of Chinese Academy of Sciences, Beijing 100049, China
3College of Chemistry, Chemical Engineering and Biotechnology, Donghua University, Shanghai 201620, China
4Department of Gastroenterology and Hepatology, Zhongshan Hospital, Fudan University, Shanghai 200032, China
5State Key Laboratory of Dairy Biotechnology, Dairy Research Institute, Bright Dairy & Food Co., Ltd, Shanghai 200436, China
6NHC Key Laboratory of Pulmonary Immune-related Diseases, Guizhou Provincial People’s Hospital, Guiyang, 550002, China
7Present address: Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden
†These authors contributed equally to this work
*Correspondence to:Xiangyan Zhang , Email:zxy35762@126.com Ronggui Hu , Email:coryhu@sibcb.ac.cn
J Mol Cell Biol, Volume 12, Issue 4, April 2020, 318-321,  https://doi.org/10.1093/jmcb/mjaa003

Dear Editor,

Enterohemorrhagic Escherichia coli (EHEC) O157:H7, a major diarrheagenic pathogen, can cause bloody diarrhea, hemorrhagic colitis, and >90% of hemolytic uremic syndrome in humans (Mead and Griffin, 1998). Many previous studies have demonstrated that O157:H7 could disrupt host ubiquitin (Ub) system by delivering virulence effectors into host cells with the type III secretion system (T3SS). NleL (also named EspX7) emerged as one of such effectors, whose E3-like activity was first identified in vitro in 2011 (Lin et al., 2011). Our recent work revealed that NleL ubiquitylates human JNK proteins and promotes EHEC-associated A/E lesions (Sheng et al., 2017). However, it remains undetermined whether NleL might mediate other microbe–host interactions that contribute to EHEC infection. Here, we demonstrate that NleL targets several components of the NF-κB pathway to suppress host NF-κB activation.



Volume 12, Issue 4
April 2020