Characterizing the impact of CPSF30 gene disruption on TuMV infection in .

CPSF30, a key polyadenylation factor, also serves as an mA reader, playing a crucial role in determining RNA fate post-transcription. While its homologs mammals are known to be vital for viral replication and immune evasion, the full scope of CPSF30 in plant, particular in viral regulation, remains less explored. Our study demonstrates that CPSF30 significantly facilitates the infection of turnip mosaic virus (TuMV) in , as evidenced by infection experiments on the engineered mutant. Among the two isoforms, CPSF30-L, which were characterized with mA binding activity, emerged as the primary isoform responding to TuMV infection. Analysis of mA components revealed potential involvement of the mA machinery in regulating TuMV infection. In contrast, CPSF30-S exhibited distinct subcellular localization, coalescing with P-body markers (AtDCP1 and AtDCP2) in cytoplasmic granules, suggesting divergent regulatory mechanisms between the isoforms. Furthermore, comprehensive mRNA-Seq and miRNA-Seq analysis of Col-0 and mutants revealed global transcriptional reprogramming, highlighting CPSF30's role in selectively modulating gene expression during TuMV infection. In conclusion, this research underscores CPSF30's critical role in the TuMV lifecycle and sets the stage for further exploration of its function in plant viral regulation.