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Identification of the early actin-rearrangement-inducing factor gene, arif-1, from Autographa californica multicapsid nuclear polyhedrosis virus.

ABSTRACT: In response to Autographa californica multicapsid nuclear polyhedrosis virus (AcMNPV) infection, a sequential rearrangement of the actin cytoskeleton occurs. Previous studies suggest that the penetration of nucleocapsids induces early actin cables followed by further changes of the actin cytoskeleton which depend on early viral gene expression. By transfection of a plasmid library into Trichoplusia ni TN-368 cells, we have identified an early viral gene, designated arif-1, that is able to induce actin rearrangement. The determination of the nucleotide sequence of arif-1 revealed one open reading frame potentially encoding a gene product of 45 kDa with no significant sequence homology to known proteins. After expression of arif-1 in transfected cells, the induced actin rearrangement, visualized by fluorescence microscopy, was comparable to the changes of the actin cytoskeleton at 3 to 7 h postinfection. These changes are based on early viral gene expression during the infection cycle. A causal link between arif-1 expression and actin rearrangement in infected cells is suggested by infection studies with the AcMNPV/Spodoptera frugiperda MNPV hybrid, which carries a deletion in the arif-1 gene. In transfection experiments the presence of the known viral transactivator IE1 was required in addition to ARIF-1 to induce actin rearrangement. IE1 was needed for promoter activation of the arif-1 gene, since arif-1 expression under the control of the early pe38 promoter was sufficient to induce actin rearrangement in transfected cells. Primer extension analyses showed that the arif-1 gene is transcribed only during the early phase of AcMNPV infection in T. ni TN-368 cells. There was a delay of about 1 h compared to ie1 transcription, which is in agreement with the assumption that IE1 transactivates the arif-1 promoter during infection.

SUBMITTER: Roncarati R

PROVIDER: S-EPMC192151 | biostudies-other | 1997 Oct

REPOSITORIES: biostudies-other

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Identification of the early actin-rearrangement-inducing factor gene, arif-1, from Autographa californica multicapsid nuclear polyhedrosis virus.

Roncarati R R Knebel-Mörsdorf D D

Journal of virology 19971001 10

In response to Autographa californica multicapsid nuclear polyhedrosis virus (AcMNPV) infection, a sequential rearrangement of the actin cytoskeleton occurs. Previous studies suggest that the penetration of nucleocapsids induces early actin cables followed by further changes of the actin cytoskeleton which depend on early viral gene expression. By transfection of a plasmid library into Trichoplusia ni TN-368 cells, we have identified an early viral gene, designated arif-1, that is able to induce ...[more]

PMID: 9311884

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Project description:As a virus-encoded actin nucleation promoting factor (NPF), P78/83 induces actin polymerization to assist in Autographa californica multiple nucleopolyhedrovirus (AcMNPV) propagation. According to our previous study, although P78/83 actively undergoes ubiquitin-independent proteasomal degradation, AcMNPV encodes budded virus/occlusion derived virus (BV/ODV)-C42 (C42), which allows P78/83 to function as a stable NPF by inhibiting its degradation during viral infection. However, whether there are other viral proteins involved in regulating P78/83-induced actin polymerization has yet to be determined. In this study, we found that Ac102, an essential viral gene product previously reported to play a key role in mediating the nuclear accumulation of actin during AcMNPV infection, is a novel regulator of P78/83-induced actin polymerization. By characterizing an ac102 knockout bacmid, we demonstrated that Ac102 participates in regulating nuclear actin polymerization as well as the morphogenesis and distribution of capsid structures in the nucleus. These regulatory effects are heavily dependent on an interaction between Ac102 and C42. Further investigation revealed that Ac102 binds to C42 to suppress K48-linked ubiquitination of C42, which decreases C42 proteasomal degradation and consequently allows P78/83 to function as a stable NPF to induce actin polymerization. Thus, Ac102 and C42 form a regulatory cascade to control viral NPF activity, representing a sophisticated mechanism for AcMNPV to orchestrate actin polymerization in both a ubiquitin-dependent and ubiquitin-independent manner.IMPORTANCE Actin is one of the most functionally important proteins in eukaryotic cells. Morphologically, actin can be found in two forms: a monomeric form called globular actin (G-actin) and a polymeric form called filamentous actin (F-actin). G-actin can polymerize to form F-actin, and nucleation promoting factor (NPF) is the initiator of this process. Many viral pathogens harness the host actin polymerization machinery to assist in virus propagation. Autographa californica multiple nucleopolyhedrovirus (AcMNPV) induces actin polymerization in host cells. P78/83, a viral NPF, is responsible for this process. Previously, we identified that BV/ODV-C42 (C42) binds to P78/83 and protects it from degradation. In this report, we determined that another viral protein, Ac102, is involved in modulating C42 ubiquitination and, consequently, ensures P78/83 activity as an NPF to initiate actin polymerization. This regulatory cascade represents a novel mechanism by which a virus can harness the cellular actin cytoskeleton to assist in viral propagation.

Dataset Information

Identification of the early actin-rearrangement-inducing factor gene, arif-1, from Autographa californica multicapsid nuclear polyhedrosis virus.

Publications

Identification of the early actin-rearrangement-inducing factor gene, arif-1, from Autographa californica multicapsid nuclear polyhedrosis virus.

Similar Datasets

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