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Vesicular stomatitis virus inhibits mitotic progression and triggers cell death
Author(s) -
Chakraborty Papia,
Seemann Joachim,
Mishra Ram K,
Wei JenHsuan,
Weil Lauren,
Nussenzveig Daniel R,
Heiber Joshua,
Barber Glen N,
Dasso Mary,
Fontoura Beatriz M A
Publication year - 2009
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.1038/embor.2009.179
Subject(s) - mitosis , vesicular stomatitis virus , biology , microbiology and biotechnology , oncolytic virus , programmed cell death , mitotic catastrophe , metaphase , rhabdoviridae , virology , virus , apoptosis , genetics , chromosome , gene
Vesicular stomatitis virus (VSV) infects and kills a wide range of cell types; however, the mechanisms involved in VSV‐mediated cell death are not fully understood. Here we show that VSV infection interferes with mitotic progression, resulting in cell death. This effect requires the interaction of VSV matrix (M) protein with the Rae1–Nup98 complex in mitosis, which is associated with a subset of ribonucleoproteins (RNPs). VSV displaced Rae1 from spindle poles, caused spindle abnormalities and triggered substantial cell death during metaphase. These effects were attenuated in cells infected with VSV expressing a mutant M protein that does not bind efficiently to the Rae1–Nup98–RNP complex. In cells that progressed to late mitosis, M protein prevented proper nuclear formation and chromatin decondensation. VSV is an oncolytic (anti‐tumour) agent as it preferentially replicates and kills tumour cells. As tumour cells have a high mitotic index, VSV‐mediated mitotic cell death probably contributes to its oncolytic activity.