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The HTLV-1 Rex protein induces nuclear accumulation of unspliced viral RNA by avoiding intron excision and
1Institut für Klinische und Molekulare Virologie der Universität Erlangen-Nürnberg, Germany.
Abstract:
The human T-cell leukemia virus (HTLV-1) Rex protein is essential for the cytoplasmic accumulation of incompletely spliced transcripts that code for the viral structural proteins. In this study effects of Rex on the amounts of total, spliced and unspliced RNA from HTLV-1 were determined. In transfected fibroblasts Rex production resulted in reduced amounts of spliced RNA and increased quantities of unspliced RNA in the nucleus. However, the total amount of viral RNA was not affected and the stability of spliced transcripts was not changed, thus indicating that only the rate of splicing was reduced. Rex action also reduced splicing in immortalized human cord blood T-cells. However, the total amount of viral transcripts and the stability of unspliced RNA in these cells were also increased in the presence of Rex. This indicates that Rex also prevents the degradation of unspliced transcripts in T-cells. The changes in the relative amounts of spliced and unspliced RNA induced by Rex were observed not only in the cytoplasm but also in the nucleus. Thus Rex affects the nucleocytoplasmic transport, splicing and stability of HTLV-1 RNA in the nucleus. These observations may suggest that Rex directs the unspliced viral RNA to the cytoplasm via a nuclear compartment that is not accessible to splicing and degradation factors.
Insights
The human T-cell leukemia virus (HTLV-1) Rex protein impacts viral RNA processing. Rex reduces splicing and prevents degradation of unspliced RNA, influencing its nuclear and cytoplasmic presence.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- The human T-cell leukemia virus (HTLV-1) Rex protein regulates viral gene expression.
- Rex is crucial for the accumulation of incompletely spliced viral transcripts in the cytoplasm.
Purpose of the Study:
- To investigate the effects of the HTLV-1 Rex protein on viral RNA processing, including splicing, stability, and nucleocytoplasmic transport.
- To elucidate the mechanisms by which Rex influences the levels of spliced and unspliced HTLV-1 RNA.
Main Methods:
- Transfection of fibroblasts and immortalized human cord blood T-cells with HTLV-1 constructs.
- Quantification of total, spliced, and unspliced HTLV-1 RNA.
- Assessment of RNA stability.
Main Results:
- Rex protein reduced spliced RNA and increased unspliced RNA in the nucleus of transfected fibroblasts.
- Rex decreased splicing rates without affecting total viral RNA or spliced transcript stability in fibroblasts.
- In T-cells, Rex reduced splicing, increased total viral transcripts, and enhanced unspliced RNA stability, indicating prevention of degradation.
- Rex-induced changes in RNA splicing and stability were observed in both nuclear and cytoplasmic compartments.
Conclusions:
- The HTLV-1 Rex protein modulates viral RNA splicing, stability, and nucleocytoplasmic transport within the nucleus.
- Rex appears to facilitate the transport of unspliced viral RNA to the cytoplasm through a nuclear compartment resistant to splicing and degradation.