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scaffold protein RACK1A positively regulates leaf senescence by coordinating the EIN3-miR164-ORE1 transcriptional cascade in Arabidopsis

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Journal of Integrative Plant Biology 2023年第7期65卷 1703-1716页

作者： Jan Masood Wei Zhu Yajuan Fu Zhiyong Li Yeling Zhou Dong Zhang Huihui Han Yan Yan Xing Wen Hongwei Guo Jiansheng Liang Key Laboratory of Molecular Design for Plant Cell Factory of Guangdong Higher Education Institutes Institute of Plant and Food SciencesDepartment of BiologySchool of Life SciencesSouthern University of Science and Technology518055ShenzhenChina

Plants have adopted versatile scaffold proteins to facilitate the crosstalk between multiple signaling pathways. Leaf senescence is a well-programmed developmental stage that is coordinated by various external and internal signals. However,the functions of plant scaffold proteins in response to senescence signals are not well understood. Here, we report that the scaffold protein RACK1A(RECEPTOR FOR ACTIVATED C KINASE1A) participates in leaf senescence mediated by ethylene signaling via the coordination of the EIN3-miR164-ORE1 transcriptional regulatory cascade. RACK1A is a novel positive regulator of ethylene-mediated leaf senescence. The rack1a mutant exhibits delayed leaf senescence, while transgenic lines overexpressing RACK1A display early leaf senescence. Moreover, RACK1A promotes EIN3(ETHYLENE INSENSITIVE 3) protein accumulation, and directly interacts with EIN3 to enhance its DNA-binding activity. Together, they then associate with the miR164 promoter to inhibit its transcription, leading to the release of the inhibition on downstream ORE1(ORESARA 1) transcription and the promotion of leaf senescence.This study reveals a mechanistic framework by which RACK1A promotes leaf senescence via the EIN3-miR164-ORE1 transcriptional cascade, and provides a paradigm for how scaffold proteins finely tune phytohormone signaling to control plant development.

关键词： Arabidopsis ethylene signaling leaf senescence RACK1 scaffold protein transcriptional cascade

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Overproduction of OsRACK1A,an effector-targeted scaffold protein promoting OsRBOHB-mediated ROS production,confers rice floral resistance to false smut disease without yield penalty

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Molecular Plant 2022年第11期15卷 1790-1806页

作者： Guo-Bang Li Jia-Xue He Jin-Long Wu He Wang Xin Zhang Jie Liu Xiao-Hong Hu Yong Zhu Shuai Shen Yi-Fei Bai Zong-Lin Yao Xin-Xian Liu Jing-Hao Zhao De-Qiang Li Yan Li Fu Huang Yan-Yan Huang Zhi-Xue Zhao Ji-Wei Zhang Shi-Xin Zhou Yun-Peng Ji Mei Pu Peng Qin Shigui Li Xuewei Chen Jing Wang Min He Weitao Li Xian-Jun Wu Zheng-Jun Xu Wen-Ming Wang Jing Fan State Key Laboratory of Crop Gene Exploration and Utilization in Southwest China Sichuan Agricultural UniversityChengdu 611130China Rice Research Institute Sichuan Agricultural UniversityChengdu 611130China

Grain formation is fundamental for crop yield but is vulnerable to abiotic and biotic stresses.Rice grain production is threatened by the false smut fungus Ustilaginoidea virens,which specifically infects rice floral organs,disrupting fertilization and seed formation.However,little is known about the molecular mechanisms of the U.virens-rice interaction and the genetic basis of floral resistance.Here,we report that U.virens secretes a cytoplasmic effector,UvCBP1,to facilitate infection of rice flowers.Mechanistically,UvCBP1 interacts with the rice scaffold protein OsRACK1A and competes its interaction with the reduced nicotinamide adenine dinucleotide phosphate oxidase OsRBOHB,leading to inhibition of reactive oxygen species(ROS)production.Although the analysis of natural variation revealed no OsRACK1A variants that could avoid being targeted by UvCBP1,expression levels of OsRACK1A are correlated with field resistance against U.virens in rice germplasm.Overproduction of OsRACK1A restores the OsRACK1A-OsRBOHB association and promotes OsRBOHB phosphorylation to enhance ROS production,conferring rice floral resistance to U.virens without yield penalty.Taken together,our findings reveal a new pathogenic mechanism mediated by an essential effector from a flower-specific pathogen and provide a valuable genetic resource for balancing disease resistance and crop yield.

关键词： rice flower false smut fungal effector scaffold protein reactive oxygen species disease resistance

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Pathogen-inducible OsMPKKI 0.2-OsMPK6 cascade phosphorylates the Raf-like kinase OsEDRI and inhibits its scaffold function to promote rice disease resistance

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Molecular Plant 2021年第4期14卷 620-632页

作者： Haigang Ma Juan Li Ling Ma Peilun Wang Yuan Xue Ping Yin Jinghua Xiao Shiping Wang National Key Laboratory of Crop Genetic Improvement National Center of Plant Gene Research(Wuhan)Huazhong Agricultural UniversityWuhan 430070China

Mitogen-activated protein kinase(MAPK)cascades regulate a myriad of plant biological processes,including disease resistance.Plant genomes encode a large number of MAPK kinase kinases(MAPKKKs)that can be divided into two subfamilies,namely MEKK-like kinases and Raf-like kinases.Thus far,the func-tions of MEKK-like MAPKKKs have been relatively well characterized,but the roles of Raf-like MAPKKKs in.plant MAPK cascades remain less understood.Here,we report the role of OsEDR1,a Raf-like MAPKKK,in the regulation of the MAPK cascade in rice response tp the bacterial pathogen Xanthomonas oryzae pv.oryzicola(Xoc).We found that OsEDR1 inhibits OsMPKK10.2(a MAPK kinase)activity through physical interaction.Upon Xoc infection,OsMPKK10.2 is phosphorylated at S304 to activate OsMPK6(a MAPK).Interestingly,activated OsMPK6 phosphorylates OsEDR1 at S861,which destabilizes OsEDR1 and thus releases the inhibition of OsMPKK10.2,leading to increased OsMPKK10.2 activity and enhanced resistance of rice plants to Xoc.Taken together,these results provide new insights into the functions of Raf-like ki-nases in the regulation of the MAPK cascade in plant immunity.

关键词： Oryza sativa MAPK bacterial disease phosphorylation scaffold protein

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MAP Kinases in Immune Responses

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Cellular & Molecular Immunology 2005年第1期2卷 20-27页

作者： YongliangZhang ChenDong DepartmentofImmunology MDAndersonCancerCenterUniversityofTexas.HoustonTX77030.USA DepartmentofImmunology MDAndersonCancerCenterUniversityofTexas.HoustonTX77030.USA／／Correspondingto：Dr.ChenDongDepartmentofImmunology.MDAndersonCancerCenterHoustonTexas77030USA

MAP kinases are evolutionarily conserved signaling regulators from budding yeast to mammals and play essential roles in both innate and adaptive immune responses.There are three main families of MAPKs in mammals.Each of them has its own activators,inactivators,substrates and scaffolds,which altogether form a fine signaling network in response to different extracellular or intracellular stimulation.In this review,we summarize recent advances in understanding of the regulation of MAP kinases and the roles of MAP kinases in innate and adaptive immune responses.Cellular & Molecular Immunology.2005;2(1):20-27.

关键词： MAP kinase MAP kinase phosphatase scaffold protein innate immune response adaptive immune response

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Down-regulation of Preso reduces glutamate-induced excitotoxicity through differentially regulating glutamate receptors in rat cortical neurons

Down-regulation of Preso reduces glutamate-induced excitotox...

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中国神经科学学会第十届全国学术会议

作者： Peng LUO Yue-Fan YANG Xin LI Yong-Bo ZHAO Hao-Xiang XU Ming-Ming ZHAO Yan QU Zhou FEI Department of Neurosurgery Xijing HospitalFourth Military Medical University Department of Anesthesiology Xijing HospitalFourth Military Medical University

Glutamate-induced excitotoxicity is involved in many neurological diseases.Preso,as a novel scaffold protein at postsynaptic level,mediates excitatory synaptic transmission and various synaptic functions.Here,we reported that the role of Preso in regulation of glutamate-induced excitotoxicity in rat cortical neurons.Knockdown of Preso with a specific small interfering RNA（siRNA） improved neuronal viability and atteunated elevation of LDH release after glutamate treatment.Down-regulation of Preso also inhibited increase of BAX/Bcl-2 ratio and cleavage of caspase-9 and caspase-3.Although expressions of mGluR1/5,NR1,NR2A,and NR2B were not changed by knockdown of Preso,down-regulation of Preso protected neurons from lutamate-induced excitotoxicity via inhibiting mGluR and NMDAR functions.On the contrary,down-regulation of Preso neither affected the expression of GluR1 and GluR2,nor influencing the fucntion of AMPAR after glutamate treatment.These results suggest that existence of Preso promotes the induction of excitotoxicity through faciliating different glutamate receptor signahngs.Therefore,Preso might be a potential pharmacological target for preventing and treating neurological diseases.

关键词： excitotoxicity glutamte receptor scaffold protein postsynaptic density apoptosis

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