Vesicular stomatitis virus inhibits mitotic progression and triggers cell death

Chakraborty, Papia; Seemann, Joachim; Mishra, Ram Kumar; Wei, Jen Hsuan; Weil, Lauren M.; Nussenzveig, Daniel R.; Heiber, Joshua F.; Barber, Glen N.; Dasso, Mary; Fontoura, Beatriz M. A.

doi:10.1038/embor.2009.179

Cited by 25 publications

(21 citation statements)

References 18 publications

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“…It is further shown that during mitosis, Rae1 in complex with Nup98, plays an essential role in mitotic spindle assembly and mitotic checkpoint regulation (Babu et al, 2003). Through binding to Rae1, VSV M protein blocks mRNA export during interphase (Faria et al, 2005; von Kobbe et al, 2000), and interferes with mitotic progression during mitosis (Chakraborty et al, 2009). Our study on ORF10 highlights the importance of Rae1 and its interaction with Nup98 in mRNA export; two viruses from very different families both target Rae1 to inhibit mRNA export.…”

Section: Discussionmentioning

confidence: 99%

A Herpesvirus Protein Selectively Inhibits Cellular mRNA Nuclear Export

Gong

Kim

Xiao

et al. 2016

Cell Host & Microbe

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SUMMARY Nuclear mRNA export is highly regulated to ensure accurate cellular gene expression. Viral inhibition of cellular mRNA export can enhance viral access to the cellular translation machinery and prevent anti-viral protein production but is generally thought to be nonselective. We report that ORF10 of Kaposi's sarcoma associated herpesvirus (KSHV), a nuclear DNA virus, inhibits mRNA export in a transcript-selective manner to control cellular gene expression. Nuclear export inhibition by ORF10 requires an interaction with an RNA export factor, Rae1. Genome-wide analysis reveals a subset of cellular mRNAs whose nuclear export is blocked by ORF10 with the 3' untranslated regions (3' UTRs) of ORF10-targeted transcripts conferring sensitivity to export inhibition. The Rae1-ORF10 interaction is important for the virus to express viral genes and produce infectious virions. These results suggest that a nuclear DNA virus can selectively interfere with RNA export to restrict host gene expression for optimal replication.

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Section: Discussionmentioning

confidence: 99%

A Herpesvirus Protein Selectively Inhibits Cellular mRNA Nuclear Export

Gong

Kim

Xiao

et al. 2016

Cell Host & Microbe

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“…This complex can function in interphase and mitosis to inhibit mRNA export [38–42] or cause death in metaphase [43], respectively. Since tumor cells have high mitotic index, death in mitosis may contribute to VSV oncolytic function.…”

Section: Nucleoporin Action In Stress and Oncogenesis Outside The Npcmentioning

confidence: 99%

Nuclear Trafficking in Health and Disease

Mor¹,

White²,

Fontoura³

2014

Current Opinion in Cell Biology

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In eukaryotic cells, the cytoplasm and the nucleus are separated by a double-membraned nuclear envelope (NE). Thus, transport of molecules between the nucleus and the cytoplasm occurs via gateways termed the nuclear pore complexes (NPCs), which are the largest intracellular channels in nature. While small molecules can passively translocate through the NPC, large molecules are actively imported into the nucleus by interacting with receptors that bind nuclear pore complex proteins (Nups). Regulatory factors then function in assembly and disassembly of transport complexes. Signaling pathways, cell cycle, pathogens, and other physiopathological conditions regulate various constituents of the nuclear transport machinery. Here, we will discuss several findings related to modulation of nuclear transport during physiological and pathological conditions, including tumorigenesis, viral infection, and congenital syndrome. We will also explore chemical biological approaches that are being used as probes to reveal new mechanisms that regulate nucleocytoplasmic trafficking and that are serving as starting points for drug development.

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“…During mitosis, both Rae1 and Nup98 were shown to regulate spindle assembly [147,148], and VSV M protein inhibited mitosis progression via the Rae1-Nup98 complex [149]. This effect is meaningful for cancer cells, which have a high mitotic index, since VSV is an oncolytic agent that preferentially replicates and kills tumor cells rather than normal cells.…”

Section: Inhibition Of Nucleo-cytoplasmic Trafficking By Rna Virusesmentioning

confidence: 99%

Nuclear Imprisonment: Viral Strategies to Arrest Host mRNA Nuclear Export

Kuss

Mata

Zhang

et al. 2013

Viruses

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Viruses possess many strategies to impair host cellular responses to infection. Nuclear export of host messenger RNAs (mRNA) that encode antiviral factors is critical for antiviral protein production and control of viral infections. Several viruses have evolved sophisticated strategies to inhibit nuclear export of host mRNAs, including targeting mRNA export factors and nucleoporins to compromise their roles in nucleo-cytoplasmic trafficking of cellular mRNA. Here, we present a review of research focused on suppression of host mRNA nuclear export by viruses, including influenza A virus and vesicular stomatitis virus, and the impact of this viral suppression on host antiviral responses.

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Vesicular stomatitis virus inhibits mitotic progression and triggers cell death

Cited by 25 publications

References 18 publications

A Herpesvirus Protein Selectively Inhibits Cellular mRNA Nuclear Export

A Herpesvirus Protein Selectively Inhibits Cellular mRNA Nuclear Export

Nuclear Trafficking in Health and Disease

Nuclear Imprisonment: Viral Strategies to Arrest Host mRNA Nuclear Export

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