A baculovirus homolog of aCu/Znsuperoxide dismutase gene

Tomalski, Michael D.; Eldridge, Russ; Miller, Lois K.

doi:10.1016/0042-6822(91)90831-u

Cited by 64 publications

(35 citation statements)

References 26 publications

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“…We analyzed the 3= PAS of AcMNPV transcripts using a 3= RACE Illumina sequencing protocol, as described in Materials and Methods. The protocol for identifying poly(A) sites was validated by comparing our results with a variety of previously mapped polyadenylation sites (63)(64)(65)(66)(67)(68), and the PAS mapped by Illumina sequencing (see Table S4 in the supplemental material) corresponded closely to sites previously mapped by S1 nuclease protection and/or 3= RACE. For this analysis, we analyzed mRNAs isolated at times ranging from 6 to 48 h p.i.…”

Section: Resultsmentioning

confidence: 59%

The Transcriptome of the Baculovirus Autographa californica Multiple Nucleopolyhedrovirus in Trichoplusia ni Cells

Chen

Zhong

Fei

et al. 2013

J Virol

166

225

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Section: Resultsmentioning

confidence: 59%

The Transcriptome of the Baculovirus Autographa californica Multiple Nucleopolyhedrovirus in Trichoplusia ni Cells

Chen

Zhong

Fei

et al. 2013

J Virol

166

225

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“…and extending through the infection cycle (33). The viral SOD is thought to scavenge reactive oxygen species and may therefore defend the virus against ROS-mediated defensive measures of the cell (84). Of the T. ni ROS-related genes examined, only the gene encoding superoxide dismutase 2 (Mn) showed a dramatic increase in transcript levels at 6 h p.i.…”

Section: Assembly and Annotation Of The T Ni Tnms42 Transcriptomementioning

confidence: 99%

Transcriptome Responses of the Host Trichoplusia ni to Infection by the Baculovirus Autographa californica Multiple Nucleopolyhedrovirus

Chen

Zhong

Fei

et al. 2014

J Virol

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Productive infection of Trichoplusia ni cells by the baculovirus Autographa californica multiple nucleopolyhedrovirus (AcMNPV) leads to expression of ϳ156 viral genes and results in dramatic cell remodeling. How the cell transcriptome responds to viral infection was unknown due to the lack of a reference genome and transcriptome for T. ni. We used an ϳ60-Gb RNA sequencing (RNA-seq) data set from infected and uninfected T. ni cells to generate and annotate a de novo transcriptome assembly of approximately 70,322 T. ni unigenes (assembled transcripts), representing the 48-h infection cycle. Using differential gene expression analysis, we found that the majority of host transcripts were downregulated after 6 h postinfection (p.i.) and throughout the remainder of the infection. In contrast, 5.7% (4,028) of the T. ni unigenes were upregulated during the early period (0 to 6 h p.i.), followed by a decrease through the remainder of the infection cycle. Also, a small subset of genes related to metabolism and stress response showed a significant elevation of transcript levels at 18 and 24 h p.i. but a decrease thereafter. We also examined the responses of genes belonging to a number of specific pathways of interest, including stress responses, apoptosis, immunity, and protein trafficking. We identified specific pathway members that were upregulated during the early phase of the infection. Combined with the parallel analysis of AcMNPV expression, these results provide both a broad and a detailed view of how baculovirus infection impacts the host cell transcriptome to evade cellular defensive responses, to modify cellular biosynthetic pathways, and to remodel cell structure. IMPORTANCEBaculoviruses are insect-specific DNA viruses that are highly pathogenic to their insect hosts. In addition to their use for biological control of certain insects, baculoviruses also serve as viral vectors for numerous biotechnological applications, such as mammalian cell transduction and protein expression for vaccine production. While there is considerable information regarding viral gene expression in infected cells, little is known regarding responses of the host cell to baculovirus infection. In these studies, we assembled a cell transcriptome from the host Trichoplusia ni and used that transcriptome to analyze changes in host cell gene expression throughout the infection cycle. The study was performed in parallel with a prior study of changes in viral gene expression. Combined, these studies provide an unprecedented new level of detail and an overview of events in the infection cycle, and they will stimulate new experimental approaches to understand, modify, and utilize baculoviruses for a variety of applications.

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“…The reduced levels of protection observed against H 2 O 2 -induced apoptosis in p35 transfected cells compared with those obtained with wild-type AcNPV may be attributed to the involvement of other viral genes. The iap and sod genes are potential candidate genes that may have a role(s) in this process (19,20,(34)(35)(36). It is nonetheless evident that a cloned copy of the p35 gene, outside the viral context, is able to significantly intercept oxidative stress-induced apoptosis.…”

Section: Resultsmentioning

confidence: 99%

The baculovirus antiapoptotic p35 gene also functions via an oxidant-dependent pathway

Sah

Taneja

Pathak

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

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Cellular imbalance in the levels of antioxidants and reactive oxygen species resulting in apoptosis is directly associated with a number of parasitic infections, aging, and several genetic and multifactorial diseases. The baculovirus AcNPV-encoded antiapoptotic p35 gene prevents apoptosis induced by a variety of apoptotic agents in different systems. We demonstrate the ability of the p35 gene to inhibit oxidative stress-induced apoptosis. In vitro cultured Spodoptera frugiperda (Sf9) insect cells infected with wild-type AcNPV carrying the antiapoptotic p35 gene did not undergo apoptosis when subjected to oxidative stress generated by the exogenous application of oxidants or in vivo generation of reactive oxygen species or on direct exposure of cells to UV radiations. An AcNPV mutant carrying a deletion of the p35 gene failed to arrest cell death. Transfection of cells with a recombinant plasmid containing the p35 gene under the transcriptional control of a stress promoter (Drosophila hsp70) was also able to rescue cells from oxidative stress-induced cell death, demonstrating the direct involvement of P35. ESR spin-trapping studies conducted in vitro and in vivo demonstrated that P35 functions directly as an antioxidant by mopping out free radicals and consequently prevents cell death by acting at an upstream step in the reactive oxygen species-mediated cell death pathway.

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A baculovirus homolog of aCu/Znsuperoxide dismutase gene

Cited by 64 publications

References 26 publications

The Transcriptome of the Baculovirus Autographa californica Multiple Nucleopolyhedrovirus in Trichoplusia ni Cells

The Transcriptome of the Baculovirus Autographa californica Multiple Nucleopolyhedrovirus in Trichoplusia ni Cells

Transcriptome Responses of the Host Trichoplusia ni to Infection by the Baculovirus Autographa californica Multiple Nucleopolyhedrovirus

The baculovirus antiapoptotic p35 gene also functions via an oxidant-dependent pathway

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