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Updated: Dec 25, 2025

Monitoring Protein-RNA Interaction Dynamics In Vivo at High Temporal Resolution Using χCRAC
Published on: May 9, 2020
CCR4, a RNA decay factor, is hijacked by a plant cytorhabdovirus phosphoprotein to facilitate virus replication
Zhen-Jia Zhang1, Qiang Gao1, Xiao-Dong Fang1
1State Key Laboratory of Agro-Biotechnology, College of Biological Sciences, China Agricultural University, Beijing, China.
Abstract:
Carbon catabolite repression 4 (CCR4) is a conserved mRNA deadenylase regulating posttranscriptional gene expression. However, regulation of CCR4 in virus infections is less understood. Here, we characterized a pro-viral role of CCR4 in replication of a plant cytorhabdovirus, Barley yellow striate mosaic virus (BYSMV). The barley (Hordeum vulgare) CCR4 protein (HvCCR4) was identified to interact with the BYSMV phosphoprotein (P). The BYSMV P protein recruited HvCCR4 from processing bodies (PBs) into viroplasm-like bodies. Overexpression of HvCCR4 promoted BYSMV replication in plants. Conversely, knockdown of the small brown planthopper CCR4 inhibited viral accumulation in the insect vector. Biochemistry experiments revealed that HvCCR4 was recruited into N-RNA complexes by the BYSMV P protein and triggered turnover of N-bound cellular mRNAs, thereby releasing RNA-free N protein to bind viral genomic RNA for optimal viral replication. Our results demonstrate that the co-opted CCR4-mediated RNA decay facilitates cytorhabdovirus replication in plants and insects.
Insights
The study reveals that Carbon catabolite repression 4 (CCR4) promotes Barley yellow striate mosaic virus (BYSMV) replication by degrading host mRNAs. This deadenylase activity is crucial for virus propagation in both plants and insect vectors.
Area of Science:
- Molecular Biology
- Virology
- Plant Pathology
Background:
- Carbon catabolite repression 4 (CCR4) is a key mRNA deadenylase involved in posttranscriptional gene regulation.
- The role of CCR4 in virus infections, particularly in plants, remains largely unexplored.
- Understanding viral interactions with host cellular machinery is vital for developing control strategies.
Purpose of the Study:
- To investigate the role of CCR4 in the replication cycle of Barley yellow striate mosaic virus (BYSMV), a plant cytorhabdovirus.
- To elucidate the molecular mechanisms by which CCR4 influences BYSMV propagation in both plant and insect hosts.
Main Methods:
- Yeast three-hybrid assays to identify protein interactions.
- Agrobacterium-mediated transient expression assays to study protein localization and viral replication.
- RNA interference (RNAi) to knock down CCR4 expression in insect vectors.
- Biochemical assays to analyze N-RNA complex formation and mRNA turnover.
Main Results:
- Barley CCR4 (HvCCR4) interacts with the BYSMV phosphoprotein (P).
- HvCCR4 is recruited to viroplasm-like bodies and promotes BYSMV replication upon overexpression.
- Knockdown of CCR4 in the small brown planthopper vector reduces BYSMV accumulation.
- HvCCR4 triggers the turnover of cellular mRNAs bound to the viral N protein, facilitating viral RNA replication.
Conclusions:
- CCR4 plays a pro-viral role in BYSMV replication by facilitating the release of the viral N protein for genomic RNA binding.
- The co-option of CCR4-mediated RNA decay by BYSMV is a strategy to enhance viral propagation in both plant and insect hosts.
- Targeting CCR4 could be a potential strategy for controlling cytorhabdovirus infections.
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