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 Δpan2Δpan3 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.

Keywords: Magnaporthe oryzae; Pan2‐Pan3 complex; deadenylation; fungal infection; mRNA decay.