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    Home > Active Ingredient News > Study of Nervous System > Cell Journal: Bao Lan/Wang Bin reveals the molecular mechanism of axon-enriched long non-coding RNA regulating axon growth

    Cell Journal: Bao Lan/Wang Bin reveals the molecular mechanism of axon-enriched long non-coding RNA regulating axon growth

    • Last Update: 2021-05-22
    • Source: Internet
    • Author: User
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    Neurons, as a type of highly specialized cells, form dendrites and axons.

    The mRNA in the cell body of the neuron can be transported to the dendrites and axons, and participate in the regulation of the development of neurons and the establishment of neural circuits through local translation.

    The previous research work of Bao Lan's research group found that the enriched miRNAs in axons are involved in axon extension by regulating local translation in axons, suggesting that non-coding RNAs play an important role in axon development.

    Existing studies have shown that lincRNA is highly expressed in the early stages of nervous system development and has high tissue distribution specificity, but the distribution, function and mechanism of lincRNA in neuronal axons are poorly understood.

    On May 4, 2021, Researcher Bao Lan from the Center for Excellence in Molecular Cell Science (Institute of Biochemistry and Cell Biology), Chinese Academy of Sciences, and Associate Researcher Wang Bin from the Shanghai Brain Science and Brain-like Research Center, as co-corresponding authors, are in the Cell Reports journal Published online research paper titled: Axon-enriched lincRNA ALAE is required for axon elongation via regulation of local mRNA translation.

    This study revealed the mechanism by which the axon-enriched long-chain non-coding RNA ALAE competes with the RNA-binding protein KHSRP and interacts with Gap43 mRNA to regulate local translation of axons and participate in axon growth.

    This study found for the first time that long non-coding RNAs enriched in axons can be used as important regulators of axon development to participate in mRNA time-conditioning control, deepening the understanding of the function and mechanism of non-coding RNAs, and providing a new molecular mechanism for the development of the nervous system .

    The study first conducted RNA sequencing on dorsal root ganglion neurons and established lincRNA expression profiles, and found that lincRNA ALAE was highly enriched in primary sensory neuron axons.

    Further studies have found that ALAE competes with Gap43 mRNA in neuronal axons to bind to KHSRP protein, promotes the release of Gap43 mRNA from the KHSRP inhibition complex, and increases the protein level of GAP43 by increasing the local translation of GAP43, thereby promoting axon growth.

    Axon-enriched lincRNA ALAE participates in the molecular mechanism of regulating local translation and axon growth by competing with KHSRP.
    This study found for the first time that axon-enriched long non-coding RNA can be used as an important regulator of axon development to participate in mRNA conditioning control, which deepens The understanding of the function and mechanism of non-coding RNA provides a new molecular mechanism for the development of the nervous system.

    Wei Manyi and Huang Jiansong, PhD students in the Bao Lan research group of the Center for Excellence in Molecular Cells, Chinese Academy of Sciences, are the co-first authors of this article.
    Researcher Bao Lan and associate researcher Wang Bin of the Shanghai Center for Brain Science and Brain-like Research are the co-corresponding authors.

    This work was strongly supported by researcher Yang Li from the Institute of Nutrition and Health of the Chinese Academy of Sciences, researcher Cheng Hong from the Center for Molecular Cell Excellence, researcher Jiang Xingyu from Southern University of Science and Technology, and researcher Zhang Xu from the Shanghai Institute for Advanced Study of the Chinese Academy of Sciences.

    Link to the paper: https://doi.
    org/10.
    1016/j.
    celrep.
    2021.
    109053 is open to reprint this article is open to reprint: just leave a message in this article to inform 
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