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    Home > Biochemistry News > Biotechnology News > The mechanism of regulating the stability of STOP1, the plant's anti-aluminum toxic transcription factor.

    The mechanism of regulating the stability of STOP1, the plant's anti-aluminum toxic transcription factor.

    • Last Update: 2020-08-06
    • Source: Internet
    • Author: User
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    On December 17th, the Proceedings of the National Academy of Sciences (PNAS) published an online research paper by the Huang Zhaofeng Research Group of the Center for Excellence in Molecular Plant Sciences of the Chinese Academy of Sciences/Institute of Plant Physiology and Ecology at the Shanghai Plant Adversity Biology Research Center, entitled F-box protein RAE1 regulations of the stability of the aluminum-redsfactor factorSTOP1 in Arabidopsis.
    the study found the stability of the F-Box protein RAE1 regulatory anti-aluminum transcription factor STOP1 and the plant's resistance to aluminum toxicity.
    aluminum is the most abundant metal element in the earth's crust, accounting for 8%.
    in neutral or alkaline soils, aluminum mainly in the insoluble form of alumina and aluminum silicate, not toxic to plants, but in acidic soil, part of the trivalent aluminum ions are dissolved, it can inhibit plant root growth, and thus inhibit the growth of the above ground, and ultimately lead to crop production, so aluminum poisoning is considered to be the main limiting factor of crop production of acidic soil.
    because acidic soils account for more than 30% of the world's arable land, aluminum poisoning is also considered the second largest abiotic adversity after drought.
    on the other hand, some plants have evolved anti-aluminum toxic mechanism, the pattern plant amoeba mainly by secreting malic acid to chelate aluminum ions, the release of aluminum poisoning, this secretion process is mainly mediated by the anion transporter protein AtALMT1 located on the cell membrane in the root.
    C2H2 type zinc finger transcription factor STOP1 mainly through direct regulation of the expression of AtALMT1 to mediate resistance to aluminum toxicity.
    at AtALMT1's mRNA expression levels are induced by aluminum toxicity, but STOP1 mRNA expression levels are not affected by aluminum toxicity, suggesting that STOP1 may be subject to post-transcription regulation.
    to explore the post-transcription regulatory mechanism of STOP1, the study constructed a reporting gene line of atALMT1 promoter fusion with the luciferase gene (LUC), and identified and cloned the gene that regulates STOP1 by screening the altered mutants of LUC fluorescence.
    using this research strategy, the study clones a new gene, RAE1 (Regulation of AtALMT1 Expression1), that encodes a domain of F-box.
    mutations in the gene led to an increase in the expression of the downstream of STOP1, including AtALMT1, which led to raE1 mutants being more resistant to aluminum toxicity but more sensitive to low phosphorus-induced root growth inhibition, while excessive expression of RAE1 inhibited the expression of AtALMT1, was more sensitive to aluminum toxicity but less sensitive to low phosphorus.
    a series of physiological and biochemical experiments, RAE1 can interact with STOP1 and degrade stop1 protein seismonotating through ubiquitinized-26S protease pathways, thus indirectly regulating the expression of stop1 downstream genes and the response of aluminum and low phosphorus, while aluminum can stabilize the STOP1 protein in part by inhibiting RAE1 degradation STOP1.
    , STOP1 directly regulates the expression of RAE1, creating a negative feedback loop between STOP1 and RAE1.
    because RAE1 has a straight-to-source gene in all plants, and the mutation makes the plant more resistant to aluminum, which provides new strategies and means for future increases in the resistance of aluminum-toxin-sensitive crops such as soybeans to aluminum.
    Ph.D. graduate Zhang Yang, postdoctoral student Zhang Jie and doctoral student Guo Jin are the co-first authors of the paper, and researcher Huang Chaofeng is the communication author of the paper.
    the research was funded by the National Natural Science Foundation of China, the Jiangsu Distinguished Youth Fund, the Chinese Academy of Sciences Pilot Project B and the Shanghai Plant Adversity Biology Research Center.
    Source: Center for Excellence in Molecular Plant Sciences/Institute for Plant Physiology and Ecology.
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