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Genome editing reveals a role for OCT4 in human embryogenesis.

Accepted version
Peer-reviewed

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Authors

Fogarty, Norah ME 
McCarthy, Afshan 
Snijders, Kirsten E 
Powell, Benjamin E 
Kubikova, Nada 

Abstract

Despite their fundamental biological and clinical importance, the molecular mechanisms that regulate the first cell fate decisions in the human embryo are not well understood. Here we use CRISPR-Cas9-mediated genome editing to investigate the function of the pluripotency transcription factor OCT4 during human embryogenesis. We identified an efficient OCT4-targeting guide RNA using an inducible human embryonic stem cell-based system and microinjection of mouse zygotes. Using these refined methods, we efficiently and specifically targeted the gene encoding OCT4 (POU5F1) in diploid human zygotes and found that blastocyst development was compromised. Transcriptomics analysis revealed that, in POU5F1-null cells, gene expression was downregulated not only for extra-embryonic trophectoderm genes, such as CDX2, but also for regulators of the pluripotent epiblast, including NANOG. By contrast, Pou5f1-null mouse embryos maintained the expression of orthologous genes, and blastocyst development was established, but maintenance was compromised. We conclude that CRISPR-Cas9-mediated genome editing is a powerful method for investigating gene function in the context of human development.

Description

Keywords

Animals, Blastocyst, CRISPR-Cas Systems, Cell Lineage, Ectoderm, Embryo, Mammalian, Embryonic Development, Female, Gene Editing, Gene Expression Regulation, Developmental, Germ Layers, Human Embryonic Stem Cells, Humans, Male, Mice, Nanog Homeobox Protein, Octamer Transcription Factor-3, Substrate Specificity, Zygote

Journal Title

Nature

Conference Name

Journal ISSN

0028-0836
1476-4687

Volume Title

550

Publisher

Springer Science and Business Media LLC
Sponsorship
Medical Research Council (MC_PC_12009)
DW was supported by the National Institute for Health Research (NIHR) Oxford Biomedical Research Centre Programme. NK was supported by the University of Oxford Clarendon Fund. AB was supported by a British Heart Foundation PhD Studentship (FS/11/77/39327). LV was supported by core grant funding from the Wellcome Trust and Medical Research Council (PSAG028). J-SK was supported by the Institute for Basic Science (IBS-R021-D1). Work in the KKN and JMAT labs was supported by the Francis Crick Institute which receives its core funding from Cancer Research UK, the UK Medical Research Council, and the Wellcome Trust (FC001120 and FC001193).