The MYB transcription factor OsMYBxoc1 regulates resistance to Xoc by directly repressing transcription of the iron transport gene OsNRAMP5 in rice.

Bacterial leaf streak caused by Xanthomonas oryzae pv. oryzicola (Xoc) is a continuous threat to rice cultivation, leading to substantial yield losses with socioeconomic implications. Iron ions are essential mineral nutrients for plant growth, but little information is available on how they influence mechanisms of rice immunity against Xoc. Here, we investigated the role of the myeloblastosis-related (MYB) transcriptional repressor OsMYBxoc1 in modulation of rice resistance through control of iron ion transport. Overexpression of OsMYBxoc1 significantly increased rice resistance, whereas OsMYBxoc1 RNA-interference lines and knockout mutants showed the opposite result. Suppression of OsMYBxoc1 expression dampened the immune response induced by pathogen-associated molecular patterns. We demonstrated that OsMYBxoc1 binds specifically to the OsNRAMP5 promoter and represses transcription of OsNRAMP5. OsNRAMP5, a negative regulator of rice resistance to bacterial leaf streak, possesses metal ion transport activity, and inhibition of OsMYBxoc1 expression increased the iron ion content in rice. Activity of the ion-dependent HO scavenging enzyme catalase was increased in plants with suppressed expression of OsMYBxoc1 or overexpression of OsNRAMP5. We found that iron ions promoted Xoc infection and interfered with the production of reactive oxygen species induced by Xoc. The type III effector XopAK directly inhibited OsMYBxoc1 transcription, indicating that the pathogen may promote its own proliferation by relieving restriction of iron ion transport in plants. In addition, iron complemented the pathogenicity defects of the RS105_ΔXopAK mutant strain, further confirming that iron utilization by Xoc may be dependent upon XopAK. In conclusion, our study reveals a novel mechanism by which OsMYBxoc1 modulates rice resistance by regulating iron accumulation and demonstrates that Xoc can accumulate iron ions by secreting the effector XopAK to promote its own infection.