毒力
氧化应激
适应(眼睛)
生物
免疫系统
微生物学
黄单胞菌
免疫调节
细菌
基因
遗传学
生物化学
神经科学
作者
Huiya Geng,Ruyi Su,Tao Yu,Wenyao Huang,Zihan Zhou,Hongxin Zhou,Qian Su,Xia Liu,Zhiyuan Ji,Wei Guo
标识
DOI:10.1021/acs.jafc.5c00235
摘要
In Xanthomonas axonopodis pv. glycines (Xag), rpoE (encoding σE) resided within the conserved rseA-mucD operon but was dually repressed by DSF signaling and the global regulator Clp. Although H2O2 induced rpoE transcription, its expression was paradoxically downregulated by H2O2-detoxification genes (oxyR, ahpC, ahpF, catB), suggesting a potential feedback loop. Notably, the rpoE mutant exhibited attenuated soybean virulence characterized by (1) reduced cell wall-degrading enzymes (CWDEs) production, leading to diminished activation of soybean innate immunity (ROS burst, callose deposition, programmed cell death, and jasmonic acid accumulation); (2) increased H2O2 sensitivity with impaired siderophore-mediated iron acquisition; (3) failure to elicit hypersensitive response (HR) in nonhosts. Significantly, rpoE complementation fully restored virulence traits. Collectively, RpoE emerges as a central regulator orchestrating oxidative stress adaptation, stealth pathogenesis via CWDEs-mediated immune suppression, and host-specific virulence/HR elicitation in Xag through its unique network, redefining sigma factor functionality in xanthomonads and providing targets for disrupting pathogen-host interactions.
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