Pan2‐Pan3 Complex‐Mediated Deadenylation Enforces mRNA Quality Control for Infection of the Rice Blast Fungus

ABSTRACT Poly(A) tail shortening by deadenylases is a central checkpoint linking mRNA fate to eukaryotic development, yet its impact on fungal pathogenesis remains unexplored. Here, we uncover that the Pan2‐Pan3 deadenylase complex is a master regulator of infection in the rice blast fungus Magnaporthe oryzae . Pan2 and Pan3 form a catalytically active complex that localizes to P‐bodies and globally trims poly(A) tails to enforce mRNA quality control. Deletion of either or both subunits abolishes this quality‐control checkpoint, causing severe virulence loss due to arrested appressorium maturation, disrupted glycogen/lipid mobilization, and impaired autophagy. Integrating poly(A)‐seq and transcriptome profiling reveals 390 mRNAs whose poly(A) tails are ≥ 5 nt longer and whose steady‐state levels are elevated in the Δ pan2 Δ pan3 mutant; among them, ATG5 , GLS2 , and DES1 —key genes governing autophagy, ER quality control, and ROS detoxification respectively—are directly deadenylated by Pan2‐Pan3. Loss of deadenylation destabilizes these mRNAs and reduces their protein output, thereby crippling infection. Our findings establish Pan2‐Pan3 complex‐mediated deadenylation as an essential post‐transcriptional layer that orchestrates fungal virulence through stringent mRNA quality control, offering a novel target for crop protection.