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The epigenetic modifier Fam208a is required to maintain epiblast cell fitness

S. Bhargava, B. Cox, C. Polydorou, V. Gresakova, V. Korinek, H. Strnad, R. Sedlacek, TA. Epp, K. Chawengsaksophak,

. 2017 ; 7 (1) : 9322. [pub] 20170824

Jazyk angličtina Země Anglie, Velká Británie

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc19028761

Gastrulation initiates with the formation of the primitive streak, during which, cells of the epiblast delaminate to form the mesoderm and definitive endoderm. At this stage, the pluripotent cell population of the epiblast undergoes very rapid proliferation and extensive epigenetic programming. Here we show that Fam208a, a new epigenetic modifier, is essential for early post-implantation development. We show that Fam208a mutation leads to impaired primitive streak elongation and delayed epithelial-to-mesenchymal transition. Fam208a mutant epiblasts had increased expression of p53 pathway genes as well as several pluripotency-associated long non-coding RNAs. Fam208a mutants exhibited an increase in p53-driven apoptosis and complete removal of p53 could partially rescue their gastrulation block. This data demonstrates a new in vivo function of Fam208a in maintaining epiblast fitness, establishing it as an important factor at the onset of gastrulation when cells are exiting pluripotency.

Citace poskytuje Crossref.org

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$a Gastrulation initiates with the formation of the primitive streak, during which, cells of the epiblast delaminate to form the mesoderm and definitive endoderm. At this stage, the pluripotent cell population of the epiblast undergoes very rapid proliferation and extensive epigenetic programming. Here we show that Fam208a, a new epigenetic modifier, is essential for early post-implantation development. We show that Fam208a mutation leads to impaired primitive streak elongation and delayed epithelial-to-mesenchymal transition. Fam208a mutant epiblasts had increased expression of p53 pathway genes as well as several pluripotency-associated long non-coding RNAs. Fam208a mutants exhibited an increase in p53-driven apoptosis and complete removal of p53 could partially rescue their gastrulation block. This data demonstrates a new in vivo function of Fam208a in maintaining epiblast fitness, establishing it as an important factor at the onset of gastrulation when cells are exiting pluripotency.
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$a Cox, Brian $u Department of Physiology, Faculty of Medicine, University of Toronto, Ontario, Canada.
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$a Korinek, Vladimir $u Laboratory of Cell and Developmental Biology, Institute of Molecular Genetics of the CAS, v.v.i., Krc, Czech Republic.
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$a Epp, Trevor Allan $u Laboratory of Transgenic Models of Diseases, Division, BIOCEV, Institute of Molecular Genetics of the CAS, v.v.i., Vestec, Czech Republic. trevor.epp@img.cas.cz. Czech Centre for Phenogenomics, Division BIOCEV, Institute of Molecular Genetics of the CAS, v.v.i., Vestec, Czech Republic. trevor.epp@img.cas.cz.
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