ArticleScientific reports2017
Mllt10 knockout mouse model reveals critical role of Af10-dependent H3K79 methylation in midfacial development.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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7 citing papers in PubMed, 1 synthesis or guideline pooled it, 17 citations in OpenAlex.
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- Evolution of Spatial and Temporal cis-Regulatory Divergence in Sticklebacks.Molecular biology and evolution · 2023Article
- DOT-1.1 (DOT1L) deficiency inBBA advances · 2023Article
- Glycolytic activity is required for the onset of neural plate folding during neural tube closure in mouse embryos.Frontiers in cell and developmental biology · 2023Article
- Molecular cytogenetic analysis of partial monosomy 10p and trisomy 10q resulting from familial pericentric inversion (10): a first case report in Chinese population.Molecular cytogenetics · 2022Article
- Hif1α-dependent hypoxia signaling contributes to the survival of deep-layer neurons and cortex formation in a mouse model.Molecular brain · 2022Article
- Breakpoint Mapping of Symptomatic Balanced Translocations Links theJournal of clinical medicine · 2020Article
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Epigenetic regulation is required to ensure the precise spatial and temporal pattern of gene expression that is necessary for embryonic development. Although the roles of some epigenetic modifications in embryonic development have been investigated in depth, the role of methylation at lysine 79 (H3K79me) is poorly understood. Dot1L, a unique methyltransferase for H3K79, forms complexes with distinct sets of co-factors. To further understand the role of H3K79me in embryogenesis, we generated a mouse knockout of Mllt10, the gene encoding Af10, one Dot1L complex co-factor. We find homozygous Mllt10 knockout mutants (Mllt10-KO) exhibit midline facial cleft. The midfacial defects of Mllt10-KO embryos correspond to hyperterolism and are associated with reduced proliferation of mesenchyme in developing nasal processes and adjacent tissue. We demonstrate that H3K79me level is significantly decreased in nasal processes of Mllt10-KO embryos. Importantly, we find that expression of AP2α, a gene critical for midfacial development, is directly regulated by Af10-dependent H3K79me, and expression AP2α is reduced specifically in nasal processes of Mllt10-KO embryos. Suppression of H3K79me completely mimicked the Mllt10-KO phenotype. Together these data are the first to demonstrate that Af10-dependent H3K79me is essential for development of nasal processes and adjacent tissues, and consequent midfacial formation.
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