echemi logo
Product
  • Product
  • Supplier
  • Inquiry
    Home > Active Ingredient News > Study of Nervous System > Research reveals the molecular mechanism of axon-enriched long non-coding RNA regulating axon growth

    Research reveals the molecular mechanism of axon-enriched long non-coding RNA regulating axon growth

    • Last Update: 2021-05-21
    • Source: Internet
    • Author: User
    Search more information of high quality chemicals, good prices and reliable suppliers, visit www.echemi.com
    Recently, Cell Reports published online the latest research progress of the researcher Bao Lan's group at the Center for Excellence in Molecular Cell Science (Institute of Biochemistry and Cell Biology) of the Chinese Academy of Sciences-Axon-enriched lincRNA ALAE is required for axon elongation via regulation of local mRNA translation.

    This study revealed the mechanism by which 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.

    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 of the research group found that the enriched microRNA (miRNA) in axons regulates local translation in axons and participates in axon extension, suggesting that non-coding RNAs play an important role in axon development (Wang et al.
    Cell Reports, 2015; Wang & Bao, Journal of Molecular Cell Biology, 2017).

    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.

    The study conducted RNA sequencing on dorsal root ganglion neurons and established lincRNA expression profiles, and found that lincRNA ALAE is 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.

    This study found for the first time that axon-enriched lncRNA can be used as an important regulator of axon development to participate in mRNA conditioning control, deepen the understanding of the function and mechanism of non-coding RNA, and provide a new molecular mechanism for the development of the nervous system.

    Doctoral students Wei Manyi and Huang Jiansong in Bao Lan's research group are the co-first authors of the paper, and Bao Lan and associate researcher Wang Bin of the Shanghai Center for Brain Science and Brain-like Research are the co-corresponding authors of the paper.

    The research work was supported by Yang Li, a researcher at the Institute of Nutrition and Health, Chinese Academy of Sciences, Cheng Hong, a researcher at the Molecular Cell Center of Excellence, Chinese Academy of Sciences, Jiang Xingyu, a researcher at Southern University of Science and Technology, and Zhang Xu, a researcher at the Shanghai Institute for Advanced Study, Chinese Academy of Sciences.
    Funded by the leading science and technology project, the Shanghai Municipal Science and Technology Commission, and the Youth Innovation Promotion Committee of the Chinese Academy of Sciences.

    Axon-enriched lincRNA ALAE participates in the molecular mechanism of regulating local translation and axon growth by competing with KHSRP Source: Center for Excellence in Molecular and Cellular Science, Chinese Academy of Sciences
    This article is an English version of an article which is originally in the Chinese language on echemi.com and is provided for information purposes only. This website makes no representation or warranty of any kind, either expressed or implied, as to the accuracy, completeness ownership or reliability of the article or any translations thereof. If you have any concerns or complaints relating to the article, please send an email, providing a detailed description of the concern or complaint, to service@echemi.com. A staff member will contact you within 5 working days. Once verified, infringing content will be removed immediately.

    Contact Us

    The source of this page with content of products and services is from Internet, which doesn't represent ECHEMI's opinion. If you have any queries, please write to service@echemi.com. It will be replied within 5 days.

    Moreover, if you find any instances of plagiarism from the page, please send email to service@echemi.com with relevant evidence.