Department of Virology, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima 734-8551, Japan.
Virology. 2010 Sep 30;405(2):334-41. doi: 10.1016/j.virol.2010.06.031.
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.
仙台病毒（SeV）M 蛋白具有 YLDL 基序，该基序对于通过表达 M 蛋白出芽病毒样颗粒（VLPs）是必需的。我们研究了 YLDL 基序对 SeV 出芽的重要性。M 蛋白缺失的 SeV 的病毒出芽不能通过瞬时表达基序突变体 M-A2（ALDA）和 M-A4（AAAA）来挽救，并且携带这些突变的病毒在细胞培养中几乎无法繁殖。然而，从 SeV M-A2 获得了具有出芽能力的回复突变体病毒 SeV M-A2R，核苷酸测序显示该基序处存在 ALDV 序列，而不是来自 M-A2 的 ALDA 序列。M-A2R 蛋白挽救了 M 蛋白缺失的 SeV 的出芽，当与病毒 C 蛋白一起表达时形成 VLPs，并恢复了与 Alix/AIP1 的结合能力。结果表明，YLDL 基序对于病毒感染背景下的有效出芽是必需的，并表明 Alix/AIP1 参与了 SeV 的出芽。
