ArticlePlant signaling & behavior2013
CDC48 function during TMV infection: regulation of virus movement and replication by degradation?
Article in Plant signaling & behavior, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Studies on the Japanese soil-borne wheat mosaic virus movement protein highlight its ability to bind plant RNA.Virology journal · 2025Article
- Cellular Partners of Tobamoviral Movement Proteins.International journal of molecular sciences · 2025Review
- The Great Game between Plants and Viruses: A Focus on Protein Homeostasis.International journal of molecular sciences · 2023Review
- Article
- Effect of the At-CDC27a gene onFrontiers in plant science · 2022Article
- Article
- The Tomato yellow leaf curl virus V2 protein forms aggregates depending on the cytoskeleton integrity and binds viral genomic DNA.Scientific reports · 2015Article
- Experimental virus evolution reveals a role of plant microtubule dynamics and TORTIFOLIA1/SPIRAL2 in RNA trafficking.PloS one · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell-division-cycle protein 48 (CDC48) is an essential, conserved ATP-driven chaperone in eukaryotic cells, which functions in diverse cellular processes including the targeting of misfolded and aggregated proteins for degradation via proteasomal and aggresomal-autophagic pathways. We recently demonstrated that plant CDC48 localizes to and interacts with Tobacco mosaic virus (TMV) movement protein (MP) in ER-associated viral protein inclusions. Our data suggest that CDC48 participates in the clearance of these viral protein inclusions in an ER-assisted protein degradation (ERAD)-like mechanism. As TMV MP-inclusions formed at late infection stages resemble aggresomes, we here propose that TMV MP enters both, ERAD-like and aggresomal pathways in its host cells and that CDC48 coordinates these processes. Moreover, as viruses often exploit host pathways for replication and spread, we propose a model in which CDC48 functions in the degradation pathway of overaccumulating viral protein and also actively participates in the regulation of TMV replication and cell-to-cell movement.
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Registered trials
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