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A novel function for human factor C1 (HCF‐1), a host protein required for herpes simplex virus infection, in pre‐mRNA splicing
Author(s) -
Ajuh Paul,
Chusainow Janet,
Ryder Ursula,
Lamond Angus I.
Publication year - 2002
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/cdf652
Subject(s) - biology , library science , art history , management , art , computer science , economics
Human factor C1 (HCF‐1) is needed for the expression of herpes simplex virus 1 (HSV‐1) immediate‐early genes in infected mammalian cells. Here, we provide evidence that HCF‐1 is required for spliceosome assembly and splicing in mammalian nuclear extracts. HCF‐1 interacts with complexes containing splicing snRNPs in uninfected mammalian cells and is a stable component of the spliceosome complex. We show that a missense mutation in HCF‐1 in the BHK21 hamster cell line tsBN67, at the non‐permissive temperature, inhibits the protein's interaction with U1 and U5 splicing snRNPs, causes inefficient spliceosome assembly and inhibits splicing. Transient expression of wild‐type HCF‐1 in tsBN67 cells restores splicing at the non‐permissive temperature. The inhibition of splicing in tsBN67 cells correlates with the temperature‐sensitive cell cycle arrest phenotype, suggesting that HCF‐1‐dependent splicing events may be required for cell cycle progression.