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Decoding the biochemical dialogue:metabolomic insights into soybean defense strategies against diverse pathogens
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作者 Min Qiu mengjun tian +7 位作者 Yaru Sun Huaibo Li Wenwen Huang Haibing Ouyang Shaoyan Lin Chen Zhang Ming Wang Yuanchao Wang 《Science China(Life Sciences)》 SCIE CAS CSCD 2024年第10期2234-2250,共17页
Soybean,a crucial global leguminous crop,confronts persistent threats from diverse pathogens,exerting a profound impact on global yields.While genetic dimensions of soybean-pathogen interactions have garnered attentio... Soybean,a crucial global leguminous crop,confronts persistent threats from diverse pathogens,exerting a profound impact on global yields.While genetic dimensions of soybean-pathogen interactions have garnered attention,the intricate biochemical responses remain poorly elucidated.In this study,we applied targeted and untargeted liquid chromatography coupled to mass spectrometry(LC-MS)metabolite profiling to dissect the complex interplay between soybeans and five distinct pathogens.Our analysis uncovered 627 idMS/MS spectra,leading to the identification of four main modules,encompassing flavonoids,isoflavonoids,triterpenoids,and amino acids and peptides,alongside other compounds such as phenolics.Profound shifts were observed in both primary and secondary metabolism in response to pathogenic infections.Particularly notable were the bidirectional changes in total flavonoids across diverse pathogenic inoculations,while triterpenoids exhibited a general declining trend.Noteworthy among the highly inducible total flavonoids were known representative antipathogen compounds(glyceollin I),backbone forms of isoflavonoids(daidzein,genistein,glycitein,formononetin),and newly purified compounds in this study(prunin).Subsequently,we delved into the biological roles of these five compounds,validating their diverse functions against pathogens:prunin significantly inhibited the vegetative growth and virulence of Phytophthora sojae;genistein exhibited a pronounced inhibitory effect on the vegetative growth and virulence of Phomopsis longicolla;daidzein and formononetin displayed significant repressive effects on the virulence of P.longicolla.This study underscores the potent utility of metabolomic tools,providing in-depth insights into plant-pathogen interactions from a biochemical perspective.The findings not only contribute to plant pathology but also offer strategic pathways for bolstering plant resistance against diseases on a broader scale. 展开更多
关键词 METABOLOME SOYBEAN soybean-pathogens interaction secondary metabolites TRITERPENOIDS flavonoids ISOFLAVONOIDS antimicrobial compounds
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The Phytophthora effector Avh241 interacts with host NDR1-like proteins to manipulate plant immunity 被引量:6
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作者 Bo Yang Sen Yang +11 位作者 Baodian Guo Yuyin Wang Wenyue Zheng mengjun tian Kaixin Dai Zehan Liu Haonan Wang Zhenchuan Ma Yan Wang Wenwu Ye Suomeng Dong Yuanchao Wang 《Journal of Integrative Plant Biology》 SCIE CAS CSCD 2021年第7期1382-1396,共15页
Plant pathogens rely on effector proteins to suppress host innate immune responses and facilitate colonization.Although the Phytophthora sojae RxLR effector Avh241 promotes Phytophthora infection,the molecular basis o... Plant pathogens rely on effector proteins to suppress host innate immune responses and facilitate colonization.Although the Phytophthora sojae RxLR effector Avh241 promotes Phytophthora infection,the molecular basis of Avh241 virulence remains poorly understood.Here we identified non-race specific disease resistance 1(NDR1)-like proteins,the critical components in plant effector-triggered immunity(ETI)responses,as host targets of Avh241.Avh241 interacts with NDR1 in the plasma membrane and suppresses NDR1-participated ETI responses.Silencing of GmNDR1s increases the susceptibility of soybean to P.sojae infection,and overexpression of GmNDR1s reduces infection,which supports its positive role in plant immunity against P.sojae.Furthermore,we demonstrate that GmNDR1 interacts with itself,and Avh241 probably disrupts the self-association of GmNDR1.These data highlight an effective counter-defense mechanism by which a Phytophthora effector suppresses plant immune responses,likely by disturbing the function of NDR1 during infection. 展开更多
关键词 NDR1 protein Phytophthora pathogens plant immunity RXLR effector virulence target
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Fg12 ribonuclease secretion contributes to Fusarium graminearum virulence and induces plant cell death 被引量:4
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作者 Bo Yang Yuyin Wang +10 位作者 mengjun tian Kaixin Dai Wenyue Zheng Zehan Liu Sen Yang Xinyu Liu Dongya Shi Haifeng Zhang Yan Wang Wenwu Ye Yuanchao Wang 《Journal of Integrative Plant Biology》 SCIE CAS CSCD 2021年第2期365-377,共13页
Filamentous fungal pathogens secrete effectors that modulate host immunity and facilitate infection. Fusarium graminearum is an important plant pathogen responsible for various devastating diseases. However, little is... Filamentous fungal pathogens secrete effectors that modulate host immunity and facilitate infection. Fusarium graminearum is an important plant pathogen responsible for various devastating diseases. However, little is known about the function of effector proteins secreted by F. graminearum. Herein, we identified several effector candidates in the F. graminearum secretome. Among them, the secreted ribonuclease Fg12 was highly upregulated during the early stages of F. graminearum infection in soybean;its deletion compromised the virulence of F. graminearum. Transient expression of Fg12 in Nicotiana benthamiana induced cell death in a light-dependent manner. Fg12 possessed ribonuclease(RNase) activity, degrading total RNA. The enzymatic activity of Fg12 was required for its cell death-promoting effects. Importantly, the ability of Fg12 to induce cell death was independent of BAK1/SOBIR1, and treatment of soybean with recombinant Fg12 protein induced resistance to various pathogens, including F. graminearum and Phytophthora sojae. Overall, our results provide evidence that RNase effectors not only contribute to pathogen virulence but also induce plant cell death. 展开更多
关键词 cell death EFFECTOR fungal ribonuclease Fusarium graminearum VIRULENCE
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