Mouse polyomavirus infection induces lamin reorganisation
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu časopisecké články
Grantová podpora
Grantová Agentura České Republiky
Czech-BioImaging LM2018129
Ministerstvo Školství, Mládeže a Tělovýchovy
European Union - Next Generation EU, Project National Institute of Virology and Bacteriology
PubMed
39288210
PubMed Central
PMC11616003
DOI
10.1111/febs.17275
Knihovny.cz E-zdroje
- Klíčová slova
- VP1, lamin A/C, lamin B, mouse polyomavirus, viral replication centres,
- MeSH
- buněčné jádro metabolismus virologie MeSH
- fosforylace MeSH
- infekce onkogenními viry virologie patologie metabolismus genetika MeSH
- jaderná lamina * metabolismus virologie MeSH
- jaderný obal metabolismus virologie MeSH
- lamin typ A * metabolismus genetika MeSH
- lamin typ B metabolismus genetika MeSH
- myši MeSH
- polyomavirové infekce * virologie metabolismus genetika patologie MeSH
- Polyomavirus * genetika patogenita fyziologie MeSH
- replikace viru * MeSH
- virové plášťové proteiny metabolismus genetika MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- lamin typ A * MeSH
- lamin typ B MeSH
- virové plášťové proteiny MeSH
- VP1 protein, polyomavirus MeSH Prohlížeč
The nuclear lamina is a dense network of intermediate filaments beneath the inner nuclear membrane. Composed of A-type lamins (lamin A/C) and B-type lamins (lamins B1 and B2), the nuclear lamina provides a scaffold for the nuclear envelope and chromatin, thereby maintaining the structural integrity of the nucleus. A-type lamins are also found inside the nucleus where they interact with chromatin and participate in gene regulation. Viruses replicating in the cell nucleus have to overcome the nuclear envelope during the initial phase of infection and during the nuclear egress of viral progeny. Here, we focused on the role of lamins in the replication cycle of a dsDNA virus, mouse polyomavirus. We detected accumulation of the major capsid protein VP1 at the nuclear periphery, defects in nuclear lamina staining and different lamin A/C phosphorylation patterns in the late phase of mouse polyomavirus infection, but the nuclear envelope remained intact. An absence of lamin A/C did not affect the formation of replication complexes but did slow virus propagation. Based on our findings, we propose that the nuclear lamina is a scaffold for replication complex formation and that lamin A/C has a crucial role in the early phases of infection with mouse polyomavirus.
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RefSeq
J02289.1