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UAG readthrough is not increased in vivo by Moloney murine leukemia virus infection
V Berteaux1, J P Rousset, M Cassan
1URA CNRS 1354, Université Paris 11, Orsay, France.
Abstract:
Expression of the pol gene of the murine leukemia viruses is subject to translational control at the UAG termination codon of the upstream gene gag. Previous experiments have suggested that: i) Moloney murine leukemia virus infection induces a tRNA(Gln)iii) in an in vitro system using the tobacco mosaic virus as template, this tRNA is able to increase readthrough at the UAG codon [1]. Here we demonstrate that, in vivo, Moloney murine leukemia virus infection does not increase translational readthrough at either the tobacco mosaic virus or the Moloney murine leukemia virus UAG stop codons.
Insights
Moloney murine leukemia virus infection does not enhance translational readthrough at UAG stop codons in vivo. This contradicts previous in vitro findings suggesting increased readthrough activity of a specific glutamine transfer RNA (tRNA(Gln)).
Area of Science:
- Molecular Biology
- Virology
- Genetics
Background:
- Murine leukemia viruses (MLVs) exhibit translational control of gene expression.
- The gag gene's UAG termination codon regulates expression of the downstream pol gene.
- Previous in vitro studies indicated a specific glutamine transfer RNA (tRNA(Gln)) might enhance readthrough at UAG codons.
Purpose of the Study:
- To investigate whether Moloney murine leukemia virus (MMLV) infection increases translational readthrough at UAG stop codons in vivo.
- To reconcile in vitro observations with in vivo biological activity.
Main Methods:
- In vivo analysis of translational readthrough at UAG codons.
- Utilizing both tobacco mosaic virus (TMV) and MMLV UAG codons as test sites.
- Assessing the impact of MMLV infection on readthrough efficiency.
Main Results:
- MMLV infection did not significantly increase translational readthrough at the TMV UAG codon in vivo.
- MMLV infection did not significantly increase translational readthrough at the MMLV UAG codon in vivo.
- The previously suggested in vitro enhancement of readthrough by tRNA(Gln) was not observed in this in vivo system.
Conclusions:
- The proposed mechanism of increased tRNA(Gln) activity enhancing MMLV gene expression in vivo is not supported by these findings.
- Translational readthrough at the gag-pol junction in MMLV may not be regulated by changes in tRNA(Gln) levels or activity during infection.
- Further research is needed to elucidate the in vivo mechanisms of translational control in MLVs.