稻黄单胞菌
转录因子
突变体
基因
效应器
生物
化学
细胞生物学
生物化学
作者
Haimiao Zhang,Baolong Sun,Wei Wu,Yang Li,Ziyi Yin,Chongchong Lu,Hongwei Zhao,Lingguang Kong,Xinhua Ding
标识
DOI:10.1016/j.xplc.2024.100859
摘要
The bacterial leaf streak (BLS) caused by Xanthomonas oryzae pv. oryzicola (Xoc) is a continuous threat to rice cultivation leading to substantial yield losses and socio-economic implications. Iron ions are essential mineral nutrients for plant growth, but little information is available on how these ions influence the immune mechanism of rice against Xoc. Hence, we investigate the role of the MYB transcriptional repressor, OsMYBxoc1, in modulating rice resistance by controlling the transport of iron ions. The overexpression of OsMYBxoc1 significantly increased rice resistance, and the OsMYBxoc1 inhibiting expressing lines and the knockout mutants were opposite. Suppressing OsMYBxoc1 expression dampened the pathogen-associated molecular pattern (PAMP)-induced immune response. We identified that OsMYBxoc1 specifically binds to the OsNRAMP5 promoter and represses the transcription of OsNRAMP5. OsNRAMP5, a negative regulator of rice resistance to BLS, possesses metal ion transport activity. Inhibition of OsMYBxoc1 expression increased the iron ions content in rice. The ion-dependent H2O2 scavenging enzyme activity was increased in plants with OsMYBxoc1 inhibited expression and OsNRAMP5 overexpression. We found that iron ions promote Xoc infection and interferes with reactive oxygen species production induced by Xoc. The type III effector XopAK directly inhibits OsMYBxoc1 transcription, indicating that pathogen may promote its own proliferation by relieving the restriction of iron ion transport in plants. In addition, iron could complement the phenotype of RS105_ΔXopAK mutant strain's pathogenicity defects, further confirming that iron utilization by Xoc may be XopAK dependent. In conclusion, our study unveils a novel mechanism through which OsMYBxoc1 modulates rice resistance by regulating iron accumulation, whereas the Xoc can accumulate iron ions by secreting the effector XopAK to promote its own infection.
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