ArticleNature genetics2025
Maternal factor OTX2 regulates human embryonic genome activation and early development.
Article in Nature genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- The degradation of maternal RNA-binding protein 4E-T regulates translational activation to ensure maternal-to-zygotic transition in mouse embryos.Cellular and molecular life sciences : CMLS · 2026Article
- Dissecting the expression pattern during embryonic development and unveiling sustained ZGA genes with oncogenic relevance.BMC genomics · 2026Article
- Mechanisms coordinating exit from the stem cell state in mammals.Genes & development · 2026Review
- The multi-omics regulatory landscape of human early embryogenesis.Cellular and molecular life sciences : CMLS · 2026Review
- Oocyte vitrification disrupts zygotic genome activation in embryos by impairing maternal spliceosome translation and Crxos splicing.PLoS genetics · 2026Article
- Human-Mouse Chimerism for Organogenesis Without Neural or Germline Contributions.International journal of biological sciences · 2026Article
- Epigenetic remodeling during early embryonic development.Frontiers in cell and developmental biology · 2026Review
- Exit from totipotency in mammals: an epigenetic perspective.Frontiers in cell and developmental biology · 2026Review
Corrections and comments
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Authors and funding
16 authors.
Funding
Abstract
Transcription factors (TFs) are instrumental in kickstarting embryonic genome activation (EGA) in many species, yet their regulatory roles in human embryos remain poorly understood. Here, we show that OTX2, a maternally provided PRD-like homeobox TF, is required for proper human EGA and early development. At the four-cell stage, OTX2 promotes activation of key EGA genes, including TPRX1 and TPRX2, and the EGA-associated repeat HERVL-int and MLT2A1. At EGA targets, OTX2 directly binds promoters and putative enhancers, many of which overlap with Alu and MaLR repetitive elements containing the OTX2 motif, and promotes chromatin accessibility. The transcriptome and developmental defects upon OTX2 knockdown are partially rescued by overexpression of TPRX1 and TPRX2. Finally, joint knockdown of OTX2 and TPRXL, encoding another maternal PRD-like homeobox TF, exacerbates chromatin opening and EGA defects at the 8C stage. These findings establish OTX2 as a crucial maternal TF that awakes the genome at the beginning of human life.
Indexed as
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.