ArticleNature communications2023
Unreprogrammed H3K9me3 prevents minor zygotic genome activation and lineage commitment in SCNT embryos.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Genome-wide profiling of histone modifications and transcription factor binding at single-cell resolution by DeChIC-seq.Cell research · 2026Article
- ERH elicits cell lineage restriction in mammalian preimplantation development and differentiation from pluripotency via H3K9me3-heterochromatin.Nature communications · 2026Article
- Dysregulated differentiation kinetics underlie the essential role of DNA damage repair in placental development.Nature communications · 2026Article
- Knockout of kdm4aa inhibits early embryonic development in zebrafish via downregulating cyp26a1.Molecular genetics and genomics : MGG · 2026Article
- Oocyte vitrification disrupts zygotic genome activation in embryos by impairing maternal spliceosome translation and Crxos splicing.PLoS genetics · 2026Article
- Autophagy regulates the maternal-to-zygotic transition through MAP1LC3B-mediated maternal mRNA decay.Autophagy · 2026Article
- Derivation of embryonic stem cells from cloned blastocysts using improved somatic cell nuclear transfer in common marmosets.Stem cell reports · 2025Article
- Efficient Somatic Cell Nuclear Transfer by Overcoming Both Pre- and Post-Implantation Epigenetic Barriers.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Hypo-osmolarity promotes naive pluripotency by reshaping cytoskeleton and increasing chromatin accessibility.Journal of advanced research · 2025Article
- Epigenome dynamics in early mammalian embryogenesis.Nature reviews. Genetics · 2025Review
- Validation of caprine H11 and the Rosa26 platform for transgene integration via CRISPR-based system: investigations on stable transgene expression and genetic biosafety.Functional & integrative genomics · 2025Article
- USP17L promotes the 2-cell-like program through deubiquitination of H2AK119ub1 and ZSCAN4.Nature communications · 2025Article
- Setd2 overexpression rescues bivalent gene expression during SCNT-mediated ZGA.Protein & cell · 2025Article
- Ovarian Endometrioma Disrupts Oocyte-Cumulus Communication and Mitochondrial Function, With Melatonin Mitigating the Effects.Cell proliferation · 2025Article
- H3K9me3 and H3K27me3 are epigenetic barriers to somatic cell nuclear transfer in rabbits.American journal of translational research · 2025Article
- The impact of retrotransposons on zygotic genome activation and the chromatin landscape of early embryos.Annals of the New York Academy of Sciences · 2024Review
- Kick-starting the zygotic genome: licensors, specifiers, and beyond.EMBO reports · 2024Review
- Cell cycle length governs heterochromatin reprogramming during early development in non-mammalian vertebrates.EMBO reports · 2024Article
- The Dynamics of Histone Modifications during Mammalian Zygotic Genome Activation.International journal of molecular sciences · 2024Review
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Somatic cell nuclear transfer (SCNT) can be used to reprogram differentiated somatic cells to a totipotent state but has poor efficiency in supporting full-term development. H3K9me3 is considered to be an epigenetic barrier to zygotic genomic activation in 2-cell SCNT embryos. However, the mechanism underlying the failure of H3K9me3 reprogramming during SCNT embryo development remains elusive. Here, we perform genome-wide profiling of H3K9me3 in cumulus cell-derived SCNT embryos. We find redundant H3K9me3 marks are closely related to defective minor zygotic genome activation. Moreover, SCNT blastocysts show severely indistinct lineage-specific H3K9me3 deposition. We identify MAX and MCRS1 as potential H3K9me3-related transcription factors and are essential for early embryogenesis. Overexpression of Max and Mcrs1 significantly benefits SCNT embryo development. Notably, MCRS1 partially rescues lineage-specific H3K9me3 allocation, and further improves the efficiency of full-term development. Importantly, our data confirm the conservation of deficient H3K9me3 differentiation in Sertoli cell-derived SCNT embryos, which may be regulated by alternative mechanisms.
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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.