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棉铃虫核型多角体病毒 tn79 基因编码一种有功能的巯基氧化酶,能够支持缺乏巯基氧化酶 ac92 基因的美洲棉铃虫多角体病毒的复制。

The Trichoplusia ni single nucleopolyhedrovirus tn79 gene encodes a functional sulfhydryl oxidase enzyme that is able to support the replication of Autographa californica multiple nucleopolyhedrovirus lacking the sulfhydryl oxidase ac92 gene.

机构信息

Molecular, Cellular, and Developmental Biology Program, Division of Biology, Kansas State University, Manhattan, KS 66506-4901, USA.

Molecular, Cellular, and Developmental Biology Program, Division of Biology, Kansas State University, Manhattan, KS 66506-4901, USA.

出版信息

Virology. 2014 Jul;460-461:207-16. doi: 10.1016/j.virol.2014.05.006. Epub 2014 Jun 13.

Abstract

The Autographa californica multiple nucleopolyhedrovirus ac92 is a conserved baculovirus gene with homology to flavin adenine dinucleotide-linked sulfhydryl oxidases. Its product, Ac92, is a functional sulfhydryl oxidase. Deletion of ac92 results in almost negligible levels of budded virus (BV) production, defects in occlusion-derived virus (ODV) co-envelopment and their inefficient incorporation into occlusion bodies. To determine the role of sulfhydryl oxidation in the production of BV, envelopment of nucleocapsids, and nucleocapsid incorporation into occlusion bodies, the Trichoplusia ni single nucleopolyhedrovirus ortholog, tn79, was substituted for ac92. Tn79 was found to be an active sulfhydryl oxidase that substituted for Ac92, resulting in the production of infectious BV, albeit about 10-fold less than an ac92-containing virus. Tn79 rescued defects in ODV morphogenesis caused by a lack of ac92. Active Tn79 sulfhydryl oxidase activity is required for efficient BV production, ODV envelopment, and their subsequent incorporation into occlusion bodies in the absence of ac92.

摘要

棉铃虫多粒包埋型核型多角体病毒 ac92 是一个保守的杆状病毒基因,与黄素腺嘌呤二核苷酸连接的巯基氧化酶具有同源性。其产物 Ac92 是一种具有功能的巯基氧化酶。ac92 的缺失导致芽生病毒 (BV) 的产量几乎可以忽略不计,包埋衍生病毒 (ODV) 的共包埋缺陷及其不能有效地掺入包埋体中。为了确定巯基氧化在 BV 的产生、核衣壳的包被以及核衣壳掺入包埋体中的作用,取代了 ac92 的是 Trichoplusia ni 单粒包埋型核型多角体病毒的 tn79 同源物。发现 tn79 是一种活性巯基氧化酶,可以替代 Ac92,导致产生感染性 BV,尽管比含有 ac92 的病毒少约 10 倍。tn79 挽救了因缺乏 ac92 而导致的 ODV 形态发生缺陷。在缺乏 ac92 的情况下,活性 tn79 巯基氧化酶活性是高效生产 BV、ODV 包被及其随后掺入包埋体所必需的。

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