HIV-1 mRNA 3′ End Processing Is Distinctively Regulated by eIF3f, CDK11, and Splice Factor 9G8

Susana T. Valente; Greg M. Gilmartin; Krishnan Venkatarama; Gloria Arriagada; Stephen P. Goff

doi:10.1016/j.molcel.2009.10.004

HIV-1 mRNA 3′ End Processing Is Distinctively Regulated by eIF3f, CDK11, and Splice Factor 9G8

Susana T. Valente, Greg M. Gilmartin, Krishnan Venkatarama, Gloria Arriagada, Stephen P. Goff

Life Sciences School

Research output: Contribution to journal › Article › peer-review

43 Citations (Scopus)

Abstract

A genetic screen previously identified the N-terminal 91 amino acids of the eukaryotic initiation factor 3 subunit f (N91-eIF3f) as a potent inhibitor of HIV-1 replication. Overexpression of N91-eIF3f or full-length eIF3f reduced the level of HIV-1 mRNAs in the infected cell. Here we show that N91-eIF3f and eIF3f act by specifically blocking the 3′ end processing of the HIV-1 pre-mRNA both in vivo and in vitro. Furthermore, the results suggest that eIF3f mediates this restriction of HIV-1 expression through the previously unsuspected involvement of a set of factors that includes eIF3f, the SR protein 9G8, and the cyclin-dependent kinase 11 (CDK11). eIF3f affects HIV-1 3′ end processing by modulating the sequence-specific recognition of the HIV-1 pre-mRNA by 9G8.

Original language	English
Pages (from-to)	279-289
Number of pages	11
Journal	Molecular Cell
Volume	36
Issue number	2
DOIs	https://doi.org/10.1016/j.molcel.2009.10.004
Publication status	Published - 23 Oct 2009

Keywords

HUMDISEASE
PROTEINS
RNA

ASJC Scopus subject areas

Molecular Biology
Cell Biology

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10.1016/j.molcel.2009.10.004

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@article{b83af9ff91134c87815d9b8fb0f467ac,

title = "HIV-1 mRNA 3′ End Processing Is Distinctively Regulated by eIF3f, CDK11, and Splice Factor 9G8",

abstract = "A genetic screen previously identified the N-terminal 91 amino acids of the eukaryotic initiation factor 3 subunit f (N91-eIF3f) as a potent inhibitor of HIV-1 replication. Overexpression of N91-eIF3f or full-length eIF3f reduced the level of HIV-1 mRNAs in the infected cell. Here we show that N91-eIF3f and eIF3f act by specifically blocking the 3′ end processing of the HIV-1 pre-mRNA both in vivo and in vitro. Furthermore, the results suggest that eIF3f mediates this restriction of HIV-1 expression through the previously unsuspected involvement of a set of factors that includes eIF3f, the SR protein 9G8, and the cyclin-dependent kinase 11 (CDK11). eIF3f affects HIV-1 3′ end processing by modulating the sequence-specific recognition of the HIV-1 pre-mRNA by 9G8.",

keywords = "HUMDISEASE, PROTEINS, RNA",

author = "Valente, {Susana T.} and Gilmartin, {Greg M.} and Krishnan Venkatarama and Gloria Arriagada and Goff, {Stephen P.}",

note = "Funding Information: We thank Uriel Hazan, ICGM, Paris; and Jill Lahti, St. Jude Children's Research Hospital, Memphis, TN, for reagents. S.T.V. was supported by the Howard Hughes Medical Institute (HHMI), the AmfAR, and the Portuguese Ministry of Education. G.A. was supported by the PEW Latin American Scholars Program. S.P.G. is an HHMI Investigator.",

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AU - Valente, Susana T.

AU - Gilmartin, Greg M.

AU - Venkatarama, Krishnan

AU - Arriagada, Gloria

AU - Goff, Stephen P.

N1 - Funding Information: We thank Uriel Hazan, ICGM, Paris; and Jill Lahti, St. Jude Children's Research Hospital, Memphis, TN, for reagents. S.T.V. was supported by the Howard Hughes Medical Institute (HHMI), the AmfAR, and the Portuguese Ministry of Education. G.A. was supported by the PEW Latin American Scholars Program. S.P.G. is an HHMI Investigator.

PY - 2009/10/23

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N2 - A genetic screen previously identified the N-terminal 91 amino acids of the eukaryotic initiation factor 3 subunit f (N91-eIF3f) as a potent inhibitor of HIV-1 replication. Overexpression of N91-eIF3f or full-length eIF3f reduced the level of HIV-1 mRNAs in the infected cell. Here we show that N91-eIF3f and eIF3f act by specifically blocking the 3′ end processing of the HIV-1 pre-mRNA both in vivo and in vitro. Furthermore, the results suggest that eIF3f mediates this restriction of HIV-1 expression through the previously unsuspected involvement of a set of factors that includes eIF3f, the SR protein 9G8, and the cyclin-dependent kinase 11 (CDK11). eIF3f affects HIV-1 3′ end processing by modulating the sequence-specific recognition of the HIV-1 pre-mRNA by 9G8.

AB - A genetic screen previously identified the N-terminal 91 amino acids of the eukaryotic initiation factor 3 subunit f (N91-eIF3f) as a potent inhibitor of HIV-1 replication. Overexpression of N91-eIF3f or full-length eIF3f reduced the level of HIV-1 mRNAs in the infected cell. Here we show that N91-eIF3f and eIF3f act by specifically blocking the 3′ end processing of the HIV-1 pre-mRNA both in vivo and in vitro. Furthermore, the results suggest that eIF3f mediates this restriction of HIV-1 expression through the previously unsuspected involvement of a set of factors that includes eIF3f, the SR protein 9G8, and the cyclin-dependent kinase 11 (CDK11). eIF3f affects HIV-1 3′ end processing by modulating the sequence-specific recognition of the HIV-1 pre-mRNA by 9G8.

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HIV-1 mRNA 3′ End Processing Is Distinctively Regulated by eIF3f, CDK11, and Splice Factor 9G8

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Keywords

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