LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 2 of total 2

Search options

  1. Article ; Online: Ubiquitination and deubiquitination of 4E-T regulate neural progenitor cell maintenance and neurogenesis by controlling P-body formation.

    Kedia, Shreeya / Aghanoori, Mohamad-Reza / Burns, Kaylan M L / Subha, Maneesha / Williams, Laura / Wen, Pengqiang / Kopp, Drayden / Erickson, Sarah L / Harvey, Emily M / Chen, Xin / Hua, Michelle / Perez, Jose Uriel / Ishraque, Fatin / Yang, Guang

    Cell reports

    2022  Volume 40, Issue 2, Page(s) 111070

    Abstract: During embryogenesis, neural stem/progenitor cells (NPCs) proliferate and differentiate to form brain tissues. Here, we show that in the developing murine cerebral cortex, the balance between the NPC maintenance and differentiation is coordinated by ... ...

    Abstract During embryogenesis, neural stem/progenitor cells (NPCs) proliferate and differentiate to form brain tissues. Here, we show that in the developing murine cerebral cortex, the balance between the NPC maintenance and differentiation is coordinated by ubiquitin signals that control the formation of processing bodies (P-bodies), cytoplasmic membraneless organelles critical for cell state regulation. We find that the deubiquitinase Otud4 and the E3 ligase Trim56 counter-regulate the ubiquitination status of a core P-body protein 4E-T to orchestrate the assembly of P-bodies in NPCs. Aberrant induction of 4E-T ubiquitination promotes P-body assembly in NPCs and causes a delay in their cell cycle progression and differentiation. In contrast, loss of 4E-T ubiquitination abrogates P-bodies and results in premature neurogenesis. Thus, our results reveal a critical role of ubiquitin-dependent regulation of P-body formation in NPC maintenance and neurogenesis during brain development.
    MeSH term(s) Animals ; Mice ; Neural Stem Cells/cytology ; Neural Stem Cells/metabolism ; Neurogenesis ; Nucleocytoplasmic Transport Proteins/metabolism ; Processing Bodies/metabolism ; Ubiquitination ; Ubiquitins/metabolism
    Chemical Substances Nucleocytoplasmic Transport Proteins ; Ubiquitins
    Language English
    Publishing date 2022-07-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2022.111070
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

  2. Article ; Online: Nucleocytoplasmic transport of the RNA-binding protein CELF2 regulates neural stem cell fates.

    MacPherson, Melissa J / Erickson, Sarah L / Kopp, Drayden / Wen, Pengqiang / Aghanoori, Mohamad-Reza / Kedia, Shreeya / Burns, Kaylan M L / Vitobello, Antonio / Tran Mau-Them, Frederic / Thomas, Quentin / Gold, Nina B / Brucker, William / Amlie-Wolf, Louise / Gripp, Karen W / Bodamer, Olaf / Faivre, Laurence / Muona, Mikko / Menzies, Lara / Baptista, Julia /
    Guegan, Katie / Male, Alison / Wei, Xing-Chang / He, Guiqiong / Long, Quan / Innes, A Micheil / Yang, Guang

    Cell reports

    2021  Volume 35, Issue 10, Page(s) 109226

    Abstract: The development of the cerebral cortex requires balanced expansion and differentiation of neural stem/progenitor cells (NPCs), which rely on precise regulation of gene expression. Because NPCs often exhibit transcriptional priming of cell-fate- ... ...

    Abstract The development of the cerebral cortex requires balanced expansion and differentiation of neural stem/progenitor cells (NPCs), which rely on precise regulation of gene expression. Because NPCs often exhibit transcriptional priming of cell-fate-determination genes, the ultimate output of these genes for fate decisions must be carefully controlled in a timely fashion at the post-transcriptional level, but how that is achieved is poorly understood. Here, we report that de novo missense variants in an RNA-binding protein CELF2 cause human cortical malformations and perturb NPC fate decisions in mice by disrupting CELF2 nucleocytoplasmic transport. In self-renewing NPCs, CELF2 resides in the cytoplasm, where it represses mRNAs encoding cell fate regulators and neurodevelopmental disorder-related factors. The translocation of CELF2 into the nucleus releases mRNA for translation and thereby triggers NPC differentiation. Our results reveal that CELF2 translocation between subcellular compartments orchestrates mRNA at the translational level to instruct cell fates in cortical development.
    MeSH term(s) CELF Proteins/metabolism ; Cell Differentiation ; Humans ; Nerve Tissue Proteins/metabolism ; Neural Stem Cells/metabolism ; RNA-Binding Proteins/metabolism
    Chemical Substances CELF Proteins ; CELF2 protein, human ; Nerve Tissue Proteins ; RNA-Binding Proteins
    Language English
    Publishing date 2021-06-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2021.109226
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

To top