ArticleScientific reports2017
Baculovirus infection induces disruption of the nuclear lamina.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Baculoviruses exploit the mitotic kinase CDK1 to disrupt the nuclear lamina.PLoS pathogens · 2026Article
- Dynamic Post-translational Modifications of Nuclear Lamins in Cellular Function and Pathophysiology.Sub-cellular biochemistry · 2025Review
- Autographa californica multiple nucleopolyhedrovirusJournal of virology · 2024Article
- A CRM1-dependent nuclear export signal inJournal of virology · 2024Article
- Multifaceted interactions between host ESCRT-III and budded virus-related proteins involved in entry and egress of the baculovirus Autographa californica multiple nucleopolyhedrovirus.Journal of virology · 2024Article
- Nuclear Cytoskeleton in Virus Infection.International journal of molecular sciences · 2022Review
- Lamin post-translational modifications: emerging toggles of nuclear organization and function.Trends in biochemical sciences · 2021Review
- Review
- Dynamic chromatin accessibility profiling reveals changes in host genome organization in response to baculovirus infection.PLoS pathogens · 2020Article
- Cellular p32 Is a Critical Regulator of Porcine Circovirus Type 2 Nuclear Egress.Journal of virology · 2019Article
- Dissecting the Cell Entry Pathway of Baculovirus by Single-Particle Tracking and Quantitative Electron Microscopic Analysis.Journal of virology · 2019Article
- Article
- Autographa californica Multiple NucleopolyhedrovirusJournal of virology · 2018Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Baculovirus nucleocapsids egress from the nucleus primarily via budding at the nuclear membrane. The nuclear lamina underlying the nuclear membrane represents a substantial barrier to nuclear egress. Whether the nuclear lamina undergoes disruption during baculovirus infection remains unknown. In this report, we generated a clonal cell line, Sf9-L, that stably expresses GFP-tagged Drosophila lamin B. GFP autofluorescence colocalized with immunofluorescent anti-lamin B at the nuclear rim of Sf9-L cells, indicating GFP-lamin B was incorporated into the nuclear lamina. Meanwhile, virus was able to replicate normally in Sf9-L cells. Next, we investigated alterations to the nuclear lamina during baculovirus infection in Sf9-L cells. A portion of GFP-lamin B localized diffusely at the nuclear rim, and some GFP-lamin B was redistributed within the nucleus during the late phase of infection, suggesting the nuclear lamina was partially disrupted. Immunoelectron microscopy revealed associations between GFP-lamin B and the edges of the electron-dense stromal mattes of the virogenic stroma, intranuclear microvesicles, and ODV envelopes and nucleocapsids within the nucleus, indicating the release of some GFP-lamin B from the nuclear lamina. Additionally, GFP-lamin B phosphorylation increased upon infection. Based on these data, baculovirus infection induced lamin B phosphorylation and disruption of the nuclear lamina.
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