| Autor: |
Boris-Lawrie K; Department of Veterinary and Biomedical Sciences, University of Minnesota, Saint Paul, MN 55108, USA., Singh G; Department of Veterinary and Biomedical Sciences, University of Minnesota, Saint Paul, MN 55108, USA.; Department of Neurosurgery, University of Minnesota, Minneapolis, MN 55455, USA., Osmer PS; Department of Astronomy, The Ohio State University, Columbus, OH 43210, USA., Zucko D; Department of Veterinary and Biomedical Sciences, University of Minnesota, Saint Paul, MN 55108, USA., Staller S; Department of Biochemistry, University of Missouri, Columbia, MO 65211, USA., Heng X; Department of Biochemistry, University of Missouri, Columbia, MO 65211, USA. |
| Abstrakt: |
The acquisition of m 7 G-cap-binding proteins is now recognized as a major variable driving the form and function of host RNAs. This manuscript compares the 5'-cap-RNA binding proteins that engage HIV-1 precursor RNAs, host mRNAs, small nuclear (sn)- and small nucleolar (sno) RNAs and sort into disparate RNA-fate pathways. Before completion of the transcription cycle, the transcription start site of nascent class II RNAs is appended to a non-templated guanosine that is methylated (m 7 G-cap) and bound by hetero-dimeric CBP80-CBP20 cap binding complex (CBC). The CBC is a nexus for the co-transcriptional processing of precursor RNAs to mRNAs and the snRNA and snoRNA of spliceosomal and ribosomal ribonucleoproteins (RNPs). Just as sn/sno-RNAs experience hyper-methylation of m 7 G-cap to trimethylguanosine (TMG)-cap, so do select HIV RNAs and an emerging cohort of mRNAs. TMG-cap is blocked from Watson:Crick base pairing and disqualified from participating in secondary structure. The HIV TMG-cap has been shown to license select viral transcripts for specialized cap-dependent translation initiation without eIF4E that is dependent upon CBP80/NCBP3. The exceptional activity of HIV precursor RNAs secures their access to maturation pathways of sn/snoRNAs, canonical and non-canonical host mRNAs in proper stoichiometry to execute the retroviral replication cycle. |
