ArticlePLoS pathogens2026
MCL1 promotes porcine epidemic diarrhea virus replication by modulating arachidonic acid metabolic pathway.
Article in PLoS pathogens, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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14 authors.
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Abstract
Porcine epidemic diarrhea virus (PEDV) poses a significant threat to the global swine industry; however, the host factors that support its replication remain poorly understood. Our previous study showed that myeloid cell leukemia 1 (MCL1) is a pro-PEDV replication cellular factor through genome-scale CRISPR-Cas9-knockout (KO) screening. Nevertheless, the molecular mechanism whereby MCL1 promotes PEDV replication is unclear. In this study, we first demonstrated that MCL1 promotes PEDV replication through its BCL-2 homology (BH) domain. Deletion of MCL1 prevented arachidonic acid (AA) from undergoing β-oxidation which led to the increase of free AA and activation of its secondary metabolic pathways resulting in significant inhibition of PEDV replication. Complementation of MCL1-KO cells with a BH domain fragment of MCL1 restored β-oxidation capacity and rescued PEDV replication. In addition, we identified acyl-CoA synthetase bubblegum family member 1 (ACSBG1) as a novel metabolic regulator that binds to the N-terminus of MCL1, rather than its BH domain, and cooperates with MCL1 to facilitate AA β-oxidation. We further demonstrated that ACSBG1 and MCL1 act together as proviral factors specifically during the replication stage of PEDV infection. In summary, this work reveals a unique and concerted interaction between MCL1 and ACSBG1 that function together to promote PEDV replication by regulating the AA metabolic pathway.
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