KDEL Receptors Assist Dengue Virus Exit from the Endoplasmic Reticulum
Membrane receptors at the surface of target cells are key host factors for virion entry; however, it is unknown whether trafficking and secretion of progeny virus requires host intracellular receptors. In this study, we demonstrate that dengue virus (DENV) interacts with KDEL receptors (KDELR), which cycle between the ER and Golgi apparatus, for vesicular transport from ER to Golgi. Depletion of KDELR by siRNA reduced egress of both DENV progeny and recombinant subviral particles (RSPs). Coimmunoprecipitation of KDELR with dengue structural protein prM required three positively charged residues at the N terminus, whose mutation disrupted protein interaction and inhibited RSP transport from the ER to the Golgi. Finally, siRNA depletion of class II Arfs, which results in KDELR accumulation in the Golgi, phenocopied results obtained with mutagenized prME and KDELR knockdown. Our results have uncovered a function for KDELR as an internal receptor involved in DENV trafficking.
Membrane receptors at the surface of target cells are key host factors for virion entry; however, it is unknown whether trafficking and secretion of progeny virus requires host intracellular receptors. In this study, we demonstrate that dengue virus (DENV) interacts with KDEL receptors (KDELR), which cycle between the ER and Golgi apparatus, for vesicular transport from ER to Golgi. Depletion of KDELR by siRNA reduced egress of both DENV progeny and recombinant subviral particles (RSPs). Coimmunoprecipitation of KDELR with dengue structural protein prM required three positively charged residues at the N terminus, whose mutation disrupted protein interaction and inhibited RSP transport from the ER to the Golgi. Finally, siRNA depletion of class II Arfs, which results in KDELR accumulation in the Golgi, phenocopied results obtained with mutagenized prME and KDELR knockdown. Our results have uncovered a function for KDELR as an internal receptor involved in DENV trafficking.
Qin, Cheng Feng、Wang, Pei Gang、Kudelko, Mateusz、Siu, Yu Lam、Li, Ming Yuan、Lagache, Thibault、Sayteng, Kouxiong、Grandadam, Marc、Olivo-Marin, Jean-Christophe、Wang, Pei Gang、Siu, Yu Lam、Lagache, Thibault、Bruzzone, Roberto、Olivo-Marin, Jean-Christophe、Bruzzone, Roberto、Kwok, Kevin、Kudelko, Mateusz、Wang, Pei Gang、Bruzzone, Roberto、Li, Ming Yuan、Zhang, Jing Shu、Zhang, Jing Shu、Kwok, Kevin、Kudelko, Mateusz
分子生物学细胞生物学微生物学
P-RIBOSYLATION FACTORSENVELOPE PROTEINSECRETORY PATHWAYGOLGIMATURATIONPARTICLESREPLICATIONOMPLEXBINDINGFUSION
Qin, Cheng Feng,Wang, Pei Gang,Kudelko, Mateusz,Siu, Yu Lam,Li, Ming Yuan,Lagache, Thibault,Sayteng, Kouxiong,Grandadam, Marc,Olivo-Marin, Jean-Christophe,Wang, Pei Gang,Siu, Yu Lam,Lagache, Thibault,Bruzzone, Roberto,Olivo-Marin, Jean-Christophe,Bruzzone, Roberto,Kwok, Kevin,Kudelko, Mateusz,Wang, Pei Gang,Bruzzone, Roberto,Li, Ming Yuan,Zhang, Jing Shu,Zhang, Jing Shu,Kwok, Kevin,Kudelko, Mateusz.KDEL Receptors Assist Dengue Virus Exit from the Endoplasmic Reticulum[EB/OL].(2016-05-11)[2025-08-11].https://chinaxiv.org/abs/201605.01355.点此复制
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