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Spatial positioning of preimplantation mouse embryo cells is regulated by mTORC1 and m(7)G-cap-dependent translation at the 8-to 16-cell transition
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SYSNO ASEP 0574409 Document Type J - Journal Article R&D Document Type Journal Article Subsidiary J Článek ve WOS Title Spatial positioning of preimplantation mouse embryo cells is regulated by mTORC1 and m(7)G-cap-dependent translation at the 8-to 16-cell transition Author(s) Gahurová, Lenka (UZFG-Y) ORCID
Tománková, J. (CZ)
Černá, P. (CZ)
Bora, P. (CZ)
Kubíčková, M. (CZ)
Virnicchi, G. (CZ)
Kovačovicová, Kristina (UZFG-Y)
Potěšil, D. (CZ)
Hruška, P. (CZ)
Zdráhal, Z. (CZ)
Anger, Martin (UZFG-Y) ORCID
Šušor, Andrej (UZFG-Y) RID, ORCID
Bruce, A. W. (CZ)Article number 230081 Source Title Open Biology. - : Royal Society Publishing
Roč. 13, č. 8 (2023)Number of pages 19 s. Publication form Online - E Language eng - English Country GB - United Kingdom Keywords mTOR/mTORC1 ; EIF4EBP1/4EBP1 ; TOP-motif Subject RIV EB - Genetics ; Molecular Biology OECD category Developmental biology Method of publishing Open access Institutional support UZFG-Y - RVO:67985904 UT WOS 001044130500002 EID SCOPUS 85167370753 DOI 10.1098/rsob.230081 Annotation Preimplantation mouse embryo development involves temporal-spatial specification and segregation of three blastocyst cell lineages: trophectoderm, primitive endoderm and epiblast. Spatial separation of the outer-trophectoderm lineage from the two other inner-cell-mass (ICM) lineages starts with the 8- to 16-cell transition and concludes at the 32-cell stages. Accordingly, the ICM is derived from primary and secondary contributed cells, with debated relative EPI versus PrE potencies. We report generation of primary but not secondary ICM populations is highly dependent on temporal activation of mammalian target of Rapamycin (mTOR) during 8-cell stage M-phase entry, mediated via regulation of the 7-methylguanosine-cap (m(7)G-cap)-binding initiation complex (EIF4F) and linked to translation of mRNAs containing 5 & PRIME, UTR terminal oligopyrimidine (TOP-) sequence motifs, as knockdown of identified TOP-like motif transcripts impairs generation of primary ICM founders. However, mTOR inhibition-induced ICM cell number deficits in early blastocysts can be compensated by the late blastocyst stage, after inhibitor withdrawal, compensation likely initiated at the 32-cell stage when supernumerary outer cells exhibit molecular characteristics of inner cells. These data identify a novel mechanism specifically governing initial spatial segregation of mouse embryo blastomeres, that is distinct from those directing subsequent inner cell formation, contributing to germane segregation of late blastocyst lineages. Workplace Institute of Animal Physiology and Genetics Contact Jana Zásmětová, knihovna@iapg.cas.cz, Tel.: 315 639 554 Year of Publishing 2024 Electronic address https://royalsocietypublishing.org/doi/10.1098/rsob.230081
Number of the records: 1