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Updated: Jun 19, 2026

Using the E1A Minigene Tool to Study mRNA Splicing Changes
Published on: April 22, 2021
HIV-1 mRNA 3' end processing is distinctively regulated by eIF3f, CDK11, and splice factor 9G8
Susana T Valente1, Greg M Gilmartin, Krishnan Venkatarama
1Howard Hughes Medical Institute, College of Physicians and Surgeons, Columbia University, HHSC 1310c, 701 West 168th Street, New York, NY 10032, USA. svalente@scripps.edu
The N-terminal 91 amino acids of eukaryotic initiation factor 3 subunit f (N91-eIF3f) inhibit HIV-1 replication by blocking pre-mRNA 3' end processing. This process involves eIF3f, 9G8, and CDK11, impacting viral gene expression.
Area of Science:
- Molecular Biology
- Virology
- Genetics
Background:
- HIV-1 replication relies on precise pre-mRNA processing.
- Eukaryotic initiation factor 3 subunit f (eIF3f) has been implicated in regulating viral gene expression.
Purpose of the Study:
- To elucidate the mechanism by which N-terminal 91 amino acids of eIF3f (N91-eIF3f) inhibit HIV-1 replication.
- To identify the cellular factors involved in eIF3f-mediated restriction of HIV-1 gene expression.
Main Methods:
- In vivo and in vitro assays to assess HIV-1 pre-mRNA 3' end processing.
- Overexpression studies of N91-eIF3f and full-length eIF3f in HIV-1 infected cells.
- Analysis of protein-protein interactions and RNA binding.
Main Results:
- N91-eIF3f and full-length eIF3f specifically inhibit the 3' end processing of HIV-1 pre-mRNA.
- eIF3f mediates this inhibition through a complex involving SR protein 9G8 and cyclin-dependent kinase 11 (CDK11).
- eIF3f modulates the recognition of HIV-1 pre-mRNA by 9G8, thereby affecting processing.
Conclusions:
- eIF3f acts as a novel restriction factor for HIV-1 replication.
- The mechanism involves the interference with HIV-1 pre-mRNA 3' end processing via the eIF3f/9G8/CDK11 complex.
- Targeting this pathway could offer new therapeutic strategies against HIV-1.
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