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p38-MAPK-mediated translation regulation during early blastocyst development is required for primitive endoderm differentiation in mice

  1. 1.
    SYSNO ASEP0543951
    Document TypeJ - Journal Article
    R&D Document TypeJournal Article
    Subsidiary JČlánek ve WOS
    Titlep38-MAPK-mediated translation regulation during early blastocyst development is required for primitive endoderm differentiation in mice
    Author(s) Bora, P. (CZ)
    Gahurová, Lenka (UZFG-Y) ORCID
    Mašek, T. (CZ)
    Hauserová, A. (CZ)
    Potěšil, D. (CZ)
    Jansová, Denisa (UZFG-Y) ORCID
    Šušor, Andrej (UZFG-Y) RID, ORCID
    Zdráhal, Z. (CZ)
    Ajduk, A. (CZ)
    Pospíšek, M. (CZ)
    Bruce, A. W. (CZ)
    Article number788
    Source TitleCommunications Biology. - : Nature Publishing Group
    Roč. 4, č. 1 (2021)
    Number of pages19 s.
    Publication formOnline - E
    Languageeng - English
    CountryGB - United Kingdom
    Keywordsearly blastocyst development ; mouse
    Subject RIVEB - Genetics ; Molecular Biology
    OECD categoryDevelopmental biology
    Method of publishingOpen access
    Institutional supportUZFG-Y - RVO:67985904
    UT WOS000668739100001
    EID SCOPUS85111784798
    DOI10.1038/s42003-021-02290-z
    AnnotationSuccessful specification of the two mouse blastocyst inner cell mass (ICM) lineages (the primitive endoderm (PrE) and epiblast) is a prerequisite for continued development and requires active fibroblast growth factor 4 (FGF4) signaling. Previously, we identified a role for p38 mitogen-activated protein kinases (p38-MAPKs) during PrE differentiation, but the underlying mechanisms have remained unresolved. Here, we report an early blastocyst window of p38-MAPK activity that is required to regulate ribosome-related gene expression, rRNA precursor processing, polysome formation and protein translation. We show that p38-MAPK inhibition-induced PrE phenotypes can be partially rescued by activating the translational regulator mTOR. However, similar PrE phenotypes associated with extracellular signal-regulated kinase (ERK) pathway inhibition targeting active FGF4 signaling are not affected by mTOR activation. These data indicate a specific role for p38-MAPKs in providing a permissive translational environment during mouse blastocyst PrE differentiation that is distinct from classically reported FGF4-based mechanisms. Bora et al. show that an early blastocyst window of p38-MAPK activity regulates ribosome-related gene expression, rRNA precursor processing, polysome formation, and protein translation. This study suggests a distinct role of p38-MAPKs for providing a permissive translational environment during mouse blastocyst primitive endoderm differentiation.
    WorkplaceInstitute of Animal Physiology and Genetics
    ContactJana Zásmětová, knihovna@iapg.cas.cz, Tel.: 315 639 554
    Year of Publishing2022
    Electronic addresshttps://www.nature.com/articles/s42003-021-02290-z
Number of the records: 1  

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