Hu, H.; Maeshima, H.; Tsukahara, R.; Ashida, A.; Kano, K.; Mishiro-Sato, E.; CHIBA, S.; Takemoto, D.; Sato, I.

Successful infection by the rice blast fungus Pyricularia oryzae depends on precise developmental transitions on the plant surface, yet the extracellular metabolites that regulate these events remain poorly understood. One such metabolite, 2'-deoxyuridine (dU), has been identified as a self-produced infection-promoting factor, but its mode of action has remained unclear. Exogenous dU did not significantly affect conidial germination but accelerated early appressorium initiation and promoted appressorium maturation, as indicated by increased glycogen mobilization and elevated intracellular turgor. Extracellular dU was detected during early infection-related development, indicating that dU accumulates under conditions conducive to appressorium formation. To test whether microbial turnover of dU influences pathogenicity, dU-degrading bacteria were isolated from rice field environments, and Enterobacter sp. strain C3 was identified as the most active isolate. Biochemical and structural analyses identified the responsible enzyme as the thymidine phosphorylase DeoA, which converts dU to uracil in a phosphate-dependent reaction. Recombinant DeoA reproduced this activity in vitro, and enzymatic depletion of dU attenuated invasive hyphal growth and lesion development. Appressorium-specific expression of deoA in P. oryzae likewise reduced pathogenicity. Together, these results identify extracellular dU as a factor promoting infection-related development in P. oryzae and suggest that dU degradation provides a potential approach for the biological control of rice blast disease.