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Combination of Oleic Acid and the gp41 Fusion Peptide Switches the Phosphatidylethanolamine-Induced Membrane Fusion Mechanism from a Nonclassical to a Classical Stalk Model
The Journal of Physical Chemistry B ( IF 2.8 ) Pub Date : 2022-05-17 , DOI: 10.1021/acs.jpcb.2c00307 Ankita Joardar 1 , Gourab Prasad Pattnaik 1 , Hirak Chakraborty 1
The Journal of Physical Chemistry B ( IF 2.8 ) Pub Date : 2022-05-17 , DOI: 10.1021/acs.jpcb.2c00307 Ankita Joardar 1 , Gourab Prasad Pattnaik 1 , Hirak Chakraborty 1
Affiliation
Membrane fusion is considered to be one of the crucial processes for the existence of eukaryotes and the entry of enveloped viruses into host cells. The fusion mechanism depends on the lipid composition of the membrane as well as the properties of fusion proteins or peptides. The gp41 fusion peptide from the human immunodeficiency virus (HIV) is known to catalyze membrane fusion by altering the physical properties of the membrane. Earlier, we demonstrated that a membrane containing 30 mol % phosphatidylethanolamine (PE) circumvents the classical stalk model because of its intrinsic negative curvature. In this work, we demonstrated how the gp41 fusion peptide influences the fusion mechanism of 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC)/1,2-dioleoyl-sn-glycero-3-phos-pho¬ethanolamine (DOPE) (70/30 mol %) membranes. We further evaluated the effect of the same peptide on the mechanism of fusion for membranes containing 30 mol % PE and a fatty acid with an intrinsic positive curvature (oleic acid (OA)). Our results show that gp41 switches the fusion mechanism from a nonclassical to a classical stalk model when membranes contain OA, but fails to do so for DOPC/DOPE membranes. This could be due to the extreme influence of the intrinsic negative curvature of PE, which is partially downregulated in the presence of OA.
中文翻译:
油酸和 gp41 融合肽的组合将磷脂酰乙醇胺诱导的膜融合机制从非经典模型转换为经典茎模型
膜融合被认为是真核生物存在和包膜病毒进入宿主细胞的关键过程之一。融合机制取决于膜的脂质组成以及融合蛋白或肽的性质。已知来自人类免疫缺陷病毒 (HIV) 的 gp41 融合肽通过改变膜的物理特性来催化膜融合。早些时候,我们证明了含有 30 mol% 磷脂酰乙醇胺 (PE) 的膜由于其固有的负曲率而绕过了经典的茎模型。在这项工作中,我们展示了 gp41 融合肽如何影响 1,2-dioleoyl - sn -glycero-3-phosphocholine (DOPC)/1,2-dioleoyl- sn的融合机制。-glycero-3-phos-pho-ethanolamine (DOPE) (70/30 mol %) 膜。我们进一步评估了相同肽对含有 30 mol% PE 和具有内在正曲率的脂肪酸(油酸 (OA))的膜融合机制的影响。我们的研究结果表明,当膜含有 OA 时,gp41 将融合机制从非经典模型转换为经典茎模型,但对于 DOPC/DOPE 膜却没有这样做。这可能是由于 PE 的内在负曲率的极端影响,在 OA 存在下部分下调。
更新日期:2022-05-17
中文翻译:
油酸和 gp41 融合肽的组合将磷脂酰乙醇胺诱导的膜融合机制从非经典模型转换为经典茎模型
膜融合被认为是真核生物存在和包膜病毒进入宿主细胞的关键过程之一。融合机制取决于膜的脂质组成以及融合蛋白或肽的性质。已知来自人类免疫缺陷病毒 (HIV) 的 gp41 融合肽通过改变膜的物理特性来催化膜融合。早些时候,我们证明了含有 30 mol% 磷脂酰乙醇胺 (PE) 的膜由于其固有的负曲率而绕过了经典的茎模型。在这项工作中,我们展示了 gp41 融合肽如何影响 1,2-dioleoyl - sn -glycero-3-phosphocholine (DOPC)/1,2-dioleoyl- sn的融合机制。-glycero-3-phos-pho-ethanolamine (DOPE) (70/30 mol %) 膜。我们进一步评估了相同肽对含有 30 mol% PE 和具有内在正曲率的脂肪酸(油酸 (OA))的膜融合机制的影响。我们的研究结果表明,当膜含有 OA 时,gp41 将融合机制从非经典模型转换为经典茎模型,但对于 DOPC/DOPE 膜却没有这样做。这可能是由于 PE 的内在负曲率的极端影响,在 OA 存在下部分下调。