Dolnik Olga, Kolesnikova Larissa, Welsch Sonja, Strecker Thomas, Schudt Gordian, Becker Stephan
Institut für Virologie, Philipps Universität Marburg, Marburg, Germany.
EMBL Structural and Computational Biology Unit, Heidelberg, Germany.
PLoS Pathog. 2014 Oct 16;10(10):e1004463. doi: 10.1371/journal.ppat.1004463. eCollection 2014 Oct.
Endosomal sorting complex required for transport (ESCRT) machinery supports the efficient budding of Marburg virus (MARV) and many other enveloped viruses. Interaction between components of the ESCRT machinery and viral proteins is predominantly mediated by short tetrapeptide motifs, known as late domains. MARV contains late domain motifs in the matrix protein VP40 and in the genome-encapsidating nucleoprotein (NP). The PSAP late domain motif of NP recruits the ESCRT-I protein tumor susceptibility gene 101 (Tsg101). Here, we generated a recombinant MARV encoding NP with a mutated PSAP late domain (rMARV(PSAPmut)). rMARV(PSAPmut) was attenuated by up to one log compared with recombinant wild-type MARV (rMARV(wt)), formed smaller plaques and exhibited delayed virus release. Nucleocapsids in rMARV(PSAPmut)-infected cells were more densely packed inside viral inclusions and more abundant in the cytoplasm than in rMARV(wt)-infected cells. A similar phenotype was detected when MARV-infected cells were depleted of Tsg101. Live-cell imaging analyses revealed that Tsg101 accumulated in inclusions of rMARV(wt)-infected cells and was co-transported together with nucleocapsids. In contrast, rMARV(PSAPmut) nucleocapsids did not display co-localization with Tsg101, had significantly shorter transport trajectories, and migration close to the plasma membrane was severely impaired, resulting in reduced recruitment into filopodia, the major budding sites of MARV. We further show that the Tsg101 interacting protein IQGAP1, an actin cytoskeleton regulator, was recruited into inclusions and to individual nucleocapsids together with Tsg101. Moreover, IQGAP1 was detected in a contrail-like structure at the rear end of migrating nucleocapsids. Down regulation of IQGAP1 impaired release of MARV. These results indicate that the PSAP motif in NP, which enables binding to Tsg101, is important for the efficient actin-dependent transport of nucleocapsids to the sites of budding. Thus, the interaction between NP and Tsg101 supports several steps of MARV assembly before virus fission.
转运所需的内体分选复合体(ESCRT)机制支持马尔堡病毒(MARV)及许多其他包膜病毒的有效出芽。ESCRT机制的组分与病毒蛋白之间的相互作用主要由短四肽基序介导,这些基序被称为晚期结构域。MARV在基质蛋白VP40和基因组包装核蛋白(NP)中含有晚期结构域基序。NP的PSAP晚期结构域基序招募ESCRT-I蛋白肿瘤易感基因101(Tsg101)。在此,我们构建了一种编码具有突变PSAP晚期结构域的NP的重组MARV(rMARV(PSAPmut))。与重组野生型MARV(rMARV(wt))相比,rMARV(PSAPmut)的毒力减弱了一个对数级,形成的蚀斑更小,且病毒释放延迟。与rMARV(wt)感染的细胞相比,rMARV(PSAPmut)感染的细胞中的核衣壳在病毒包涵体内堆积更密集,在细胞质中数量更多。当MARV感染的细胞中Tsg101缺失时,检测到类似的表型。活细胞成像分析显示,Tsg101在rMARV(wt)感染细胞的包涵体中积累,并与核衣壳一起共转运。相比之下,rMARV(PSAPmut)核衣壳与Tsg101不共定位,其转运轨迹显著缩短,靠近质膜的迁移严重受损,导致向丝状伪足(MARV的主要出芽位点)的募集减少。我们进一步表明,Tsg101相互作用蛋白IQGAP1(一种肌动蛋白细胞骨架调节剂)与Tsg101一起被募集到包涵体和单个核衣壳中。此外,在迁移的核衣壳后端的类似轨迹样结构中检测到IQGAP1。IQGAP1的下调会损害MARV的释放。这些结果表明,NP中的PSAP基序能够与Tsg101结合,对核衣壳有效依赖肌动蛋白转运至出芽位点很重要。因此,NP与Tsg101之间的相互作用在病毒分裂之前支持了MARV组装的多个步骤。