Characterizing the impact of CPSF30 gene disruption on TuMV infection in Arabidopsis thaliana

Abstract

CPSF30, a key polyadenylation factor, also serves as an m 6 A 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 Arabidopsis thaliana , as evidenced by infection experiments on the engineered cpsf30 mutant. Among the two isoforms, CPSF30-L, which were characterized with m 6 A binding activity, emerged as the primary isoform responding to TuMV infection. Analysis of m 6 A components revealed potential involvement of the m 6 A 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 cpsf30 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.