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Setosphaeria turcica ATR turns off appressorium‐mediated maize infection and triggers melanin‐involved self‐protection in response to genotoxic stress

机译:斜纹夜蛾ATR可以关闭食堂介导的玉米感染并响应基因毒性胁迫触发涉及黑色素的自我保护

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摘要

Eukaryotic organisms activate conserved signalling networks to maintain genomic stability in response to DNA genotoxic stresses. However, the coordination of this response pathway in fungal pathogens remains largely unknown. In the present study, we investigated the mechanism by which the northern corn leaf blight pathogen controls maize infection and activates self‐protection pathways in response to DNA genotoxic insults. Appressorium‐mediated maize infection by was blocked by the S‐phase checkpoint. This repression was dependent on the checkpoint central kinase Ataxia Telangiectasia and Rad3 related (ATR), as inhibition of ATR activity or knockdown of the gene recovered appressorium formation in the presence of genotoxic reagents. ATR promoted melanin biosynthesis in as a defence response to stress. The melanin biosynthesis genes and were induced by the ATR‐mediated S‐phase checkpoint. The responses to DNA genotoxic stress were conserved in a wide range of phytopathogenic fungi, including , , , and , which are known causal agents for plant diseases. We propose that in response to genotoxic stress, phytopathogenic fungi including activate an ATR‐dependent pathway to suppress appressorium‐mediated infection and induce melanin‐related self‐protection in addition to conserved responses in eukaryotes.
机译:真核生物可激活保守的信号网络,以响应DNA遗传毒性应激而维持基因组稳定性。然而,在真菌病原体中这种应答途径的协调仍然是未知的。在本研究中,我们研究了北部玉米叶枯病病原体控制玉米感染并响应DNA遗传毒性损害而激活自我保护途径的机制。 S期检查站阻止了Appressorium介导的玉米感染。这种抑制作用取决于检查点中心激酶共济失调毛细血管扩张症和与Rad3相关的(ATR),因为在存在基因毒性试剂的情况下,抑制ATR活性或敲低基因恢复了前庭的形成。 ATR促进了黑色素的生物合成,作为对压力的防御反应。黑色素的生物合成基因是由ATR介导的S期检查点诱导的。对DNA遗传毒性胁迫的反应在多种植物病原真菌(包括,,和)中得以保留,这是已知的植物病害病原体。我们提出,针对遗传毒性胁迫,除真核生物中的保守应答外,植物病原性真菌还包括激活ATR依赖性途径来抑制ress介导的感染并诱导黑色素相关的自我保护。

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