{"doi":"10.1101/2025.10.09.680815","title":"mRNA poly(A)-tail length is a battleground for coronavirus–host competition","abstract":"Abstract Most eukaryotic mRNAs contain a poly(A) tail, which in post-embryonic cells enhances their stability. Many cytoplasmic RNA viruses also harbor poly(A) tails on their genomic RNA and mRNAs. Here, we report that coronavirus infection causes cytoplasmic poly(A)-binding protein (PABPC) activity to become limiting, which preferentially destabilizes short-tailed host mRNAs, occurring before the action of virally encoded mRNA-decay factor nsp1. In this environment hostile to poly(A) tails, viral RNAs maintain a narrow tail-length distribution centering on 70–80 nucleotides across infection cycles. They do this through two mechanisms. First, viral tails are extended during RNA synthesis within double-membrane vesicles; second, viral tails are capped by a complex that includes PABPC1 and CSDE1 and slows tail shortening. Our findings suggest poly(A)-tail length is an arena of host– virus conflict, in which preserving tail lengths of viral mRNAs promotes their cytoplasmic dominance. Highlights PABPC1 becomes limiting during coronavirus infection Limiting PABPC1 promotes decay of short-tailed host mRNAs—independently of nsp1 The tail lengths of coronaviral mRNAs are extended during their synthesis in DMVs Viral tails are capped by PABPC1 and CSDE1, which protects against deadenylation","journal":"bioRxiv (Cold Spring Harbor Laboratory)","year":2025,"id":555783,"datarank":0.2138954178394579,"base_score":1.3862943611198906,"endowment":1.3862943611198906,"self_citation_contribution":0.20794415416798362,"citation_network_contribution":0.005951263671474277,"self_endowment_contribution":0.20794415416798362,"citer_contribution":0.005951263671474277,"corpus_percentile":null,"corpus_rank":null,"citation_count":3,"citer_count":2,"citers_with_citation_signal":1,"citers_with_endowment":1,"datacite_reuse_total":0,"is_dataset":false,"is_dataset_confidence":0.958,"is_data_producer":false,"deposit_databanks":null,"is_oa":true,"file_count":0,"downloads":0,"has_version_chain":false,"published_date":"2025-01-01","fair_score":null,"fair_percentile":null,"algorithm_id":"datarank_citation_only_1hop_v6","ranking_scope":"data_only","authors":[{"id":563406,"name":"Yevgen Levdansky","orcid":"0000-0003-0708-0771","position":1,"is_corresponding":false},{"id":891543,"name":"Amer Balabaki","orcid":"0000-0002-1509-886X","position":2,"is_corresponding":false},{"id":72857,"name":"Sherry S. Y. Nyeo","orcid":null,"position":3,"is_corresponding":false},{"id":308735,"name":"Eugene Valkov","orcid":"0000-0002-3721-1739","position":4,"is_corresponding":false},{"id":59206,"name":"David P. Bartel","orcid":"0000-0002-3872-2856","position":5,"is_corresponding":false},{"id":1001812,"name":"Arash Latifkar","orcid":"0000-0001-8682-1077","position":0,"is_corresponding":true}],"reference_count":96,"raw_metadata":{"citation_network_status":"fetched"},"created_at":"2026-07-19T02:55:03.976486Z","pmid":"41279592","pmcid":null,"fwci":null,"citation_percentile":null,"influential_citations":0,"oa_status":null,"license":null,"views":0,"total_file_size_bytes":0,"version_count":0,"fair_f":null,"fair_a":null,"fair_i":null,"fair_r":null,"fair_zscore":null,"fair_rationale":null,"fair_model":null,"fair_agent_version":null,"fair_fulltext_source":null,"fair_has_llm":null,"fair_computed_at":null,"clinical_trials":[],"software_tools":[],"db_accessions":[],"linked_datasets":[],"topics":[]}