Li Zhaofei, Blissard Gary W
Boyce Thompson Institute at Cornell University, Ithaca, New York 14853-1801, USA.
J Virol. 2009 May;83(9):4447-61. doi: 10.1128/JVI.02252-08. Epub 2009 Feb 25.
GP64, the major envelope glycoprotein of the Autographa californica multicapsid nucleopolyhedrovirus budded virion, is important for host cell receptor binding and mediates low-pH-triggered membrane fusion during entry by endocytosis. Previous transmembrane (TM) domain replacement studies showed that the TM domain serves a critical role in GP64 function. To extend the prior studies and examine specific sequence requirements of the TM domain, we generated a variety of GP64 TM domain mutations. The mutations included 4- to 8-amino-acid deletions, as well as single and multiple point mutations. While most TM domain deletion constructs remained fusion competent, those containing deletions of eight amino acids from the C terminus did not mediate detectable fusion. The addition of a hydrophobic amino acid (A, L, or V) to the C terminus of construct C8 (a construct that contains a TM domain deletion of eight amino acids from the C terminus) restored fusion activity. These data suggest that the membrane fusion function of GP64 is dependent on a critical length of the hydrophobic TM domain. All GP64 proteins with a truncated TM domain mediated detectable virion budding with dramatically lower levels of efficiency than wild-type GP64. The effects of deletions of various lengths and positions in the TM domain were also examined for their effects on viral infectivity. Further analysis of the TM domain by single amino acid substitutions and 3-alanine scanning mutations identified important but not essential amino acid positions. These studies showed that amino acids at positions 485 to 487 and 503 to 505 are important for cell surface expression of GP64, while amino acids at positions 483 to 484 and 494 to 496 are important for virus budding. Overall, our results show that specific features and amino acid sequences, particularly the length of the hydrophobic TM domain, play critical roles in membrane anchoring, membrane fusion, virus budding, and infectivity.
GP64是苜蓿银纹夜蛾多核衣壳核型多角体病毒出芽病毒粒子的主要包膜糖蛋白,对于宿主细胞受体结合很重要,并在内吞作用进入过程中介导低pH触发的膜融合。先前的跨膜(TM)结构域置换研究表明,TM结构域在GP64功能中起关键作用。为了扩展先前的研究并检查TM结构域的特定序列要求,我们产生了多种GP64 TM结构域突变。这些突变包括4至8个氨基酸的缺失,以及单点和多点突变。虽然大多数TM结构域缺失构建体仍具有融合能力,但那些从C末端缺失8个氨基酸的构建体未介导可检测到的融合。在构建体C8(一个从C末端包含8个氨基酸的TM结构域缺失的构建体)的C末端添加一个疏水氨基酸(A、L或V)恢复了融合活性。这些数据表明,GP64的膜融合功能取决于疏水TM结构域的关键长度。所有具有截短TM结构域的GP64蛋白介导了可检测到的病毒粒子出芽,但效率远低于野生型GP64。还检查了TM结构域中不同长度和位置的缺失对病毒感染性的影响。通过单氨基酸取代和丙氨酸扫描突变对TM结构域进行进一步分析,确定了重要但非必需的氨基酸位置。这些研究表明,485至487位和503至505位的氨基酸对于GP64的细胞表面表达很重要,而483至484位和494至496位的氨基酸对于病毒出芽很重要。总体而言,我们的结果表明,特定特征和氨基酸序列,特别是疏水TM结构域的长度,在膜锚定、膜融合、病毒出芽和感染性中起关键作用。