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Hepadnaviral polymerase (P) suppresses translation: implication for coordinated switch from translation to encapsidation
Author(s) -
Ryu Dongkyun,
Ryu WangShick
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a651
Subject(s) - polysome , translation (biology) , biology , translational regulation , rna , internal ribosome entry site , polymerase , protein biosynthesis , five prime untranslated region , genetics , messenger rna , replicon , polyadenylation , ribosome , microbiology and biotechnology , genome , gene
The pregenomic RNA (pgRNA) of hepadnaviruses serves not only as mRNA for the translation of C (core) and P (polymerase) proteins, but also as an RNA template for the viral genome replication. These two processes (translation and genome replication) are most likely mutually exclusive, as 5′end proximal stem‐loop structure (encapsidation signal orε) is critical for encapsidation, whereas such secondary structure would be disrupted by scanning ribosomes. Then a question arises as to how these two apparently competing processes are coordinated. Considering the fact that the P‐ ε interaction is prerequisite for encapsidation, we hypothesized that the viral P protein could act as a translational suppressor. To address the hypothesis, we monitored the C ORF translation upon the P protein overexpression. Consistent with the hypothesis, we found that the P protein suppresses the C ORF translation via its binding to 5′ ε sequence. Further, polysome distribution analysis revealed that the P protein significantly reduced the mRNA abundance in the polysome fractions, directly demonstrating the impact of the P protein on ongoing translation. Importantly, the translation suppression by the P protein was also observed in the replicon context, a finding that underscores its physiological relevance. We speculated that the translational suppression might lead to the coordinated switch from translation to genome replication.