Kiwifruit bacterial canker,caused by Pseudomonas syringae pv.actinidiae(Psa),is a significant threat to the kiwifruit industry.The two-component signaling systems(TCSs) play a crucial role in regulating the virulence ...Kiwifruit bacterial canker,caused by Pseudomonas syringae pv.actinidiae(Psa),is a significant threat to the kiwifruit industry.The two-component signaling systems(TCSs) play a crucial role in regulating the virulence of P.syringae,yet their specific function in Psa remains largely unclear.In this study,we found that disrupting the TCS RegAB(encoded by Psa 802/Psa_ 803) resulted in a notable increase in the virulence of P.syringae pv.actinidiae M228(Psa M228) in host plant and hypersensitive reaction(HR) in nonhost plant.Through comparative transcriptome analysis of the Psa M228wild-type strain and the regA mutant,we identified the pivotal role of RegAB in controlling various physiological pathways,including the type Ⅲ secretion system(T3SS),a key determinant of Psa virulence.Additionally,we discovered that the RegA has binding sites in the promoter region of the hrpR/S,and the transcriptional level of the hrpR and other T3SSrelated genes increased in the regA deletion strain relative to the Psa M228 wild-type.The DNA-binding affinity of RegA,and therefore the repressor function,is enhanced by its phosphorylation.Our findings unveil the function of TCS RegAB and the regulatory mechanism of T3SS by RegAB in Psa,highlighting the diverse functions of the RegAB system.展开更多
基金supported by the National Key Research and Development Program of China (2022YFD1400200 to Wang Yao and Yang Mingming)the National Natural Science Foundation of China (32330004 to Shen Xihui, 32170130 to Wang Yao and 32102283 to Yang Mingming)。
文摘Kiwifruit bacterial canker,caused by Pseudomonas syringae pv.actinidiae(Psa),is a significant threat to the kiwifruit industry.The two-component signaling systems(TCSs) play a crucial role in regulating the virulence of P.syringae,yet their specific function in Psa remains largely unclear.In this study,we found that disrupting the TCS RegAB(encoded by Psa 802/Psa_ 803) resulted in a notable increase in the virulence of P.syringae pv.actinidiae M228(Psa M228) in host plant and hypersensitive reaction(HR) in nonhost plant.Through comparative transcriptome analysis of the Psa M228wild-type strain and the regA mutant,we identified the pivotal role of RegAB in controlling various physiological pathways,including the type Ⅲ secretion system(T3SS),a key determinant of Psa virulence.Additionally,we discovered that the RegA has binding sites in the promoter region of the hrpR/S,and the transcriptional level of the hrpR and other T3SSrelated genes increased in the regA deletion strain relative to the Psa M228 wild-type.The DNA-binding affinity of RegA,and therefore the repressor function,is enhanced by its phosphorylation.Our findings unveil the function of TCS RegAB and the regulatory mechanism of T3SS by RegAB in Psa,highlighting the diverse functions of the RegAB system.
