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作 者:Tongtong Liu Suren Deng Cheng Zhang Xu Yang Lei Shi Fangsen Xu Sheliang Wang Chuang Wang
机构地区:[1]Microelement Research Center,College of Resources&Environment,Huazhong Agricultural University,Wuhan,430070 China [2]Key Laboratory of Arable Land Conservation(Middle and Lower Reaches of Yangtze River),Ministry of Agriculture,Huazhong Agricultural University,Wuhan,430070 China
出 处:《Journal of Integrative Plant Biology》2023年第5期1099-1112,共14页植物学报(英文版)
基 金:supported by the National Key Research and Development Program of China(2022YFD1900700);the National Natural Science Foundation of China(32072663);the Opening Project of Guangdong Provincial Key Laboratory of Quality&Safety Risk Assessment for Agroproducts(SZKF202201)。
摘 要:Inorganic phosphate(Pi)is often limited in soils due to precipitation with iron(Fe)and aluminum(Al).To scavenge heterogeneously distributed phosphorus(P)resources,plants have evolved a local Pi signaling pathway that induces malate secretion to solubilize the occluded Fe-P or Al-P oxides.In this study,we show that Pi limitation impaired brassinosteroid signaling and downregulated BRASSINAZOLE-RESISTANT 1(BZR1)expression in Arabidopsis thaliana.Exogenous 2,4-epibrassinolide treatment or constitutive activation of BZR1(in the bzr1-D mutant)significantly reduced primary root growth inhibition under Pi-starvation conditions by downregulating ALUMINUM-ACTIVATED MALATE TRANSPORTER 1(ALMT1)expression and malate secretion.Furthermore,At BZR1 competitively suppressed the activator effect of SENSITIVITY TO PROTON RHIZOTOXICITY 1(STOP1)on ALMT1 expression and malate secretion in Nicotiana benthamiana leaves and Arabidopsis.The ratio of nuclear-localized STOP1 and BZR1 determined ALMT1 expression and malate secretion in Arabidopsis.In addition,BZR1-inhibited malate secretion is conserved in rice(Oryza sativa).Our findings provide insight into plant mechanisms for optimizing the secretion of malate,an important carbon resource,to adapt to Pi-deficiency stress.
关 键 词:ALMT1 brassinosteroid signaling bzr1 MALATE phosphate deficiency STOP1
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