Significance of the YLDL motif in the M protein and Alix/AIP1 for Sendai virus budding in the context of virus infection
Significance of the YLDL motif in the M protein and Alix/AIP1 for Sendai virus budding in the context of virus infection
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DOI：
10.1016/j.virol.2010.06.031
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发表时间：
2010-09-30
期刊：
影响因子：
3.7
通讯作者：
Sakaguchi, Takemasa
中科院分区：
文献类型：
--
作者：
Irie, Takashi;Inoue, Makoto;Sakaguchi, Takemasa
仙台病毒（SeV） M蛋白具有一个YLDL基序，该基序是通过表达M蛋白使病毒样颗粒（VLPs）出芽所必需的。我们研究了YLDL基序对SeV出芽的重要性。M-A2 （ALDA）和M-A4 （AAAA）基序突变体的瞬时表达无法挽救M-A2缺陷SeV的病毒出芽，具有这些突变的病毒在培养细胞中几乎无法繁殖。然而，从SeV M-A2中获得了一种发芽能力强的逆转病毒SeV M-A2R，核苷酸测序显示基序上有ALDV序列，而不是来自M-A2的ALDA序列。M-A2R蛋白挽救了m缺陷SeV的出芽，在与病毒C蛋白表达时形成VLPs，并恢复了与Alix/AIP1结合的能力。结果表明，在病毒感染的情况下，YLDL基序对于有效出芽至关重要，并且表明Alix/AIP1参与了SeV出芽。(C) 2010爱思唯尔公司版权所有。
Sendai virus (SeV) M protein has a YLDL motif, which is essential for budding of virus-like particles (VLPs) by expression of the M protein. We investigated the importance of the YLDL motif for SeV budding. Virus budding of an M-deficient SeV was not rescued by transient expression of motif mutants, M-A2 (ALDA) and M-A4 (AAAA), and viruses possessing those mutations hardly propagated in cultured cells. However, a budding-competent revertant virus, SeV M-A2R, was obtained from SeV M-A2, and nucleotide sequencing showed an ALDV sequence at the motif instead of the ALDA sequence derived from M-A2. The M-A2R protein rescued budding of an M-deficient SeV, formed VLPs when expressed with viral C protein, and restored the capacity to bind with Alix/AIP1. The results indicate that the YLDL motif is essential for efficient budding in the context of virus infection and suggest involvement of Alix/AIP1 in SeV budding. (C) 2010 Elsevier Inc. All rights reserved.