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Determining Genome-wide Transcript Decay Rates in Proliferating and Quiescent Human Fibroblasts
Published on: January 2, 2018
Virus-mediated mRNA decay by hyperadenylation.
Kevin J Sokoloski1, Emily L Chaskey, Jeffrey Wilusz
1Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA.
Genome Biology
|August 15, 2009
Summary
Kaposi's sarcoma-associated herpesvirus infection causes cellular mRNA to degrade through hyperadenylation. This process also moves cytoplasmic poly(A)-binding proteins into the nucleus during infection.
Area of Science:
- Virology
- Molecular Biology
- Cellular Biology
Background:
- Kaposi's sarcoma-associated herpesvirus (KSHV) is a human oncogenic herpesvirus.
- KSHV infection impacts host cell gene expression and mRNA metabolism.
- Poly(A)-binding proteins (PABPs) are crucial for mRNA stability and translation.
Purpose of the Study:
- To investigate the effects of KSHV infection on cellular mRNA degradation.
- To determine the role of mRNA hyperadenylation in KSHV-induced mRNA loss.
- To examine the subcellular localization of cytoplasmic poly(A)-binding proteins during KSHV infection.
Main Methods:
- Analysis of cellular mRNA levels in KSHV-infected cells.
- Assessment of mRNA polyadenylation status using specific molecular techniques.
- Immunofluorescence microscopy to track the localization of poly(A)-binding proteins.
Main Results:
- KSHV infection leads to significant degradation of cellular mRNAs.
- Degraded transcripts exhibit a characteristic hyperadenylation pattern.
- Cytoplasmic poly(A)-binding proteins are found to relocalize to the nucleus in infected cells.
Conclusions:
- KSHV infection disrupts host mRNA homeostasis through hyperadenylation-mediated degradation.
- The nuclear relocalization of cytoplasmic poly(A)-binding proteins may contribute to altered gene expression during KSHV infection.
- Understanding these mechanisms is vital for developing targeted antiviral therapies.
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