VSV disrupts the Rae1/mrnp41 mRNA nuclear export pathway

Paula A. Faria; Papia Chakraborty; Agata Levay; Glen N. Barber; Heather J. Ezelle; Jost Enninga; Carlos Arana; Jan Van Deursen; Beatriz M A Fontoura

doi:10.1016/j.molcel.2004.11.023

VSV disrupts the Rae1/mrnp41 mRNA nuclear export pathway

Paula A. Faria, Papia Chakraborty, Agata Levay, Glen N. Barber, Heather J. Ezelle, Jost Enninga, Carlos Arana, Jan Van Deursen, Beatriz M A Fontoura

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195 Scopus citations

Abstract

Interference with nucleocytoplasmic transport is a strategy employed by certain viruses to compromise host cellular function. While it has been shown that the matrix (M) protein of the vesicular stomatitis virus (VSV) inhibits nuclear export of host cell mRNAs, the underlying mechanism has not been fully established. Here we show that VSV M protein binds the mRNA export factor Rae1/mrnp41. A mutant of M protein defective in Rae1 binding is unable to inhibit mRNA nuclear export. We further show that increased expression of Rae1 fully reverts the inhibition of mRNA export induced by M protein or following virus infection. We found that Rae1 is induced by interferon-γ, a cytokine that plays a critical role in the immune response to viruses, such as VSV. Thus, these results demonstrate that VSV M protein blocks mRNA export by disrupting Rae1 function, which can be reverted by induction of Rae1 expression.

Original language	English (US)
Pages (from-to)	93-102
Number of pages	10
Journal	Molecular cell
Volume	17
Issue number	1
DOIs	https://doi.org/10.1016/j.molcel.2004.11.023
State	Published - Jan 7 2005

ASJC Scopus subject areas

Molecular Biology
Cell Biology

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10.1016/j.molcel.2004.11.023

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@article{2daa1845d0ae49049aa8ffb4333caa8e,

title = "VSV disrupts the Rae1/mrnp41 mRNA nuclear export pathway",

abstract = "Interference with nucleocytoplasmic transport is a strategy employed by certain viruses to compromise host cellular function. While it has been shown that the matrix (M) protein of the vesicular stomatitis virus (VSV) inhibits nuclear export of host cell mRNAs, the underlying mechanism has not been fully established. Here we show that VSV M protein binds the mRNA export factor Rae1/mrnp41. A mutant of M protein defective in Rae1 binding is unable to inhibit mRNA nuclear export. We further show that increased expression of Rae1 fully reverts the inhibition of mRNA export induced by M protein or following virus infection. We found that Rae1 is induced by interferon-γ, a cytokine that plays a critical role in the immune response to viruses, such as VSV. Thus, these results demonstrate that VSV M protein blocks mRNA export by disrupting Rae1 function, which can be reverted by induction of Rae1 expression.",

author = "Faria, {Paula A.} and Papia Chakraborty and Agata Levay and Barber, {Glen N.} and Ezelle, {Heather J.} and Jost Enninga and Carlos Arana and {Van Deursen}, Jan and Fontoura, {Beatriz M A}",

note = "Funding Information: We thank G. Blobel, C. Luetje, V. Nussenzweig, J. Bixby, S. Lemmon, and K. Burnstein for productive discussions. We thank E. Izaurralde for generous gifts of VSV M protein plasmids and K. Jeganathan for generating MEF cell lines. We thank D.S. Lyles for the anti-VSV M protein antibody. We thank N. Satterly, H. Valentine, and A. Rebelo for experimental assistance. This work was supported by the NIH (R01 GM067159-01 to B.M.A.F.), a Florida Biomedical Research Grant (BM025 to B.M.A.F.), an American Cancer Society Institutional Grant (IRG98-277 to B.M.A.F.), and a Stanley J. Glaser Biomedical Research Grant (700393 to B.M.A.F.). P.C. is supported by an American Heart Association fellowship (0315123B). ",

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doi = "10.1016/j.molcel.2004.11.023",

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T1 - VSV disrupts the Rae1/mrnp41 mRNA nuclear export pathway

AU - Faria, Paula A.

AU - Chakraborty, Papia

AU - Levay, Agata

AU - Barber, Glen N.

AU - Ezelle, Heather J.

AU - Enninga, Jost

AU - Arana, Carlos

AU - Van Deursen, Jan

AU - Fontoura, Beatriz M A

N1 - Funding Information: We thank G. Blobel, C. Luetje, V. Nussenzweig, J. Bixby, S. Lemmon, and K. Burnstein for productive discussions. We thank E. Izaurralde for generous gifts of VSV M protein plasmids and K. Jeganathan for generating MEF cell lines. We thank D.S. Lyles for the anti-VSV M protein antibody. We thank N. Satterly, H. Valentine, and A. Rebelo for experimental assistance. This work was supported by the NIH (R01 GM067159-01 to B.M.A.F.), a Florida Biomedical Research Grant (BM025 to B.M.A.F.), an American Cancer Society Institutional Grant (IRG98-277 to B.M.A.F.), and a Stanley J. Glaser Biomedical Research Grant (700393 to B.M.A.F.). P.C. is supported by an American Heart Association fellowship (0315123B).

PY - 2005/1/7

Y1 - 2005/1/7

N2 - Interference with nucleocytoplasmic transport is a strategy employed by certain viruses to compromise host cellular function. While it has been shown that the matrix (M) protein of the vesicular stomatitis virus (VSV) inhibits nuclear export of host cell mRNAs, the underlying mechanism has not been fully established. Here we show that VSV M protein binds the mRNA export factor Rae1/mrnp41. A mutant of M protein defective in Rae1 binding is unable to inhibit mRNA nuclear export. We further show that increased expression of Rae1 fully reverts the inhibition of mRNA export induced by M protein or following virus infection. We found that Rae1 is induced by interferon-γ, a cytokine that plays a critical role in the immune response to viruses, such as VSV. Thus, these results demonstrate that VSV M protein blocks mRNA export by disrupting Rae1 function, which can be reverted by induction of Rae1 expression.

AB - Interference with nucleocytoplasmic transport is a strategy employed by certain viruses to compromise host cellular function. While it has been shown that the matrix (M) protein of the vesicular stomatitis virus (VSV) inhibits nuclear export of host cell mRNAs, the underlying mechanism has not been fully established. Here we show that VSV M protein binds the mRNA export factor Rae1/mrnp41. A mutant of M protein defective in Rae1 binding is unable to inhibit mRNA nuclear export. We further show that increased expression of Rae1 fully reverts the inhibition of mRNA export induced by M protein or following virus infection. We found that Rae1 is induced by interferon-γ, a cytokine that plays a critical role in the immune response to viruses, such as VSV. Thus, these results demonstrate that VSV M protein blocks mRNA export by disrupting Rae1 function, which can be reverted by induction of Rae1 expression.

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VSV disrupts the Rae1/mrnp41 mRNA nuclear export pathway

Abstract

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