The MRE11-ATM-SOG1 DNA damage signaling pathway confers rice immunity to Xanthomonas oryzae

文献类型: 外文期刊

第一作者: Xu, Zhan

作者: Xu, Zhan;Xu, Zhan;Shi, Chuanlin;Zhang, Hong;Chen, Wu;Qian, Hongge;Zhang, Zhipeng;Qian, Qian;Shang, Lianguang;Qu, Mingnan;Qiu, Jiehua;Qian, Qian;Qian, Qian;Shang, Lianguang

作者机构:

关键词: Oryza sativa; Xanthomonas oryzae pv. oryzae; DSBs; phytoalexins; MRE11-ATM-SOG1; TOP6; complex,

期刊名称:PLANT COMMUNICATIONS ( 影响因子:10.5; 五年影响因子:10.5 )

ISSN: 2590-3462

年卷期: 2024 年 5 卷 4 期

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收录情况: SCI

摘要: Plants are constantly exposed to microbial pathogens in the environment. One branch of innate plant immunity is mediated by cell -membrane -localized receptors, but less is known about associations between DNA damage and plant immune responses. Here, we show that rice ( Oryza sativa) mesophyll cells are prone to DNA double -stranded breaks (DSBs) in response to ZJ173, a strain of Xanthomonas oryzae pv. oryzae ( Xoo ). The DSB signal transducer ataxia telangiectasia mutated (ATM), but not the ATM and Rad3-related branch, confers resistance against Xoo . Mechanistically, the MRE11-ATM module phosphorylates suppressor of gamma response 1 (SOG1), which activates several phenylpropanoid pathway genes and prompts downstream phytoalexin biosynthesis during Xoo infection. Intriguingly, overexpression of the topoisomerase gene TOP6A3 causes a switch from the classic non -homologous end joining (NHEJ) pathway to the alternative NHEJ and homologous recombination pathways at Xoo- induced DSBs. The enhanced ATM signaling of the alternative NHEJ pathway strengthens the SOG1-regulated phenylpropanoid pathway and thereby boosts Xoo -induced phytoalexin biosynthesis in TOP6A3-OE1 overexpression lines. Overall, the MRE11-ATM-SOG1 pathway serves as a prime example of plant-pathogen interactions that occur via host non-specific recognition. The function of TOP6-facilitated ATM signaling in the defense response makes it a promising target for breeding of rice germplasm that exhibits resistance to bacterial blight disease without a growth penalty.

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