Enterohaemorrhagic E. coli modulates an ARF6:Rab35 signaling axis to prevent recycling endosome maturation during infection.
Enterohaemorrhagic E. coli modulates an ARF6:Rab35 signaling axis to prevent recycling endosome maturation during infection.
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DOI：
10.1016/j.jmb.2016.05.023
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发表时间：
2016-08-28
影响因子：
5.6
通讯作者：
Clements, Abigail
中科院分区：
文献类型：
--
作者：
Furniss, R. Christopher D.;Slater, Sabrina;Frankel, Gad;Clements, Abigail
关键词：
Enteropathogenic and enterohaemorrhagic Escherichia coli (EPEC/EHEC) manipulate a plethora of host cell processes to establish infection of the gut mucosa. This manipulation is achieved via the injection of bacterial effector proteins into host cells using a Type III secretion system. We have previously reported that the conserved EHEC and EPEC effector EspG disrupts recycling endosome function, reducing cell surface levels of host receptors through accumulation of recycling cargo within the host cell. Here we report that EspG interacts specifically with the small GTPases ARF6 and Rab35 during infection. These interactions target EspG to endosomes and prevent Rab35-mediated recycling of cargo to the host cell surface. Furthermore, we show that EspG has no effect on Rab35-mediated uncoating of newly formed endosomes, and instead leads to the formation of enlarged EspG/TfR/Rab11 positive, EEA1/Clathrin negative stalled recycling structures. Thus, this paper provides a molecular framework to explain how EspG disrupts recycling whilst also reporting the first known simultaneous targeting of ARF6 and Rab35 by a bacterial pathogen. EHEC delivers effector proteins into host cells to establish infection in the gut The effector EspG interacts with GTP-ARF6 confining EspG to recycling endosomes During infection EspG interacts preferentially with Rab35, not Rab1 Spatial restriction of bacterial effectors during infection determines their function
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