ArticleEpigenetics & chromatin2021
AF10 (MLLT10) prevents somatic cell reprogramming through regulation of DOT1L-mediated H3K79 methylation.
Article in Epigenetics & chromatin, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- PICALM::MLLT10 translocated leukemia.FEBS letters · 2026Review
- Single-cell omics uncover gene dynamics shaping embryonic and extra embryonic lineages in pig blastocysts.iScience · 2026Article
- From the past to the present: evolving theories in the pathophysiology of normal pressure hydrocephalus.Journal of neurology, neurosurgery, and psychiatry · 2026Review
- DOT1L activity limits transcription elongation velocity and favors RNAPII pausing to facilitate mutagenesis by AID.Nature communications · 2026Article
- Article
- Prevalence of and gene regulatory constraints on transcriptional adaptation in single cells.Genome biology · 2024Article
- The emerging role of DOT1L in cell proliferation and differentiation: Friend or foe.Histology and histopathology · 2024Review
- Genetic variation in patent foramen ovale: a case-control genome-wide association study.Frontiers in genetics · 2024Article
- DOT1L interaction partner AF10 controls patterning of H3K79 methylation and RNA polymerase II to maintain cell identity.Stem cell reports · 2023Article
- Prevalence of and gene regulatory constraints on transcriptional adaptation in single cells.bioRxiv : the preprint server for biology · 2023Article
- Phenotypic Chemical Screening in CD4Methods in molecular biology (Clifton, N.J.) · 2023Article
- Broad genomic workup including optical genome mapping uncovers aFrontiers in oncology · 2022Article
- Signals for antigen-independent differentiation of memory CD8Cellular and molecular life sciences : CMLS · 2021Review
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
backgroundThe histone H3 lysine 79 (H3K79) methyltransferase DOT1L is a key chromatin-based barrier to somatic cell reprogramming. However, the mechanisms by which DOT1L safeguards cell identity and somatic-specific transcriptional programs remain unknown.
resultsWe employed a proteomic approach using proximity-based labeling to identify DOT1L-interacting proteins and investigated their effects on reprogramming. Among DOT1L interactors, suppression of AF10 (MLLT10) via RNA interference or CRISPR/Cas9, significantly increases reprogramming efficiency. In somatic cells and induced pluripotent stem cells (iPSCs) higher order H3K79 methylation is dependent on AF10 expression. In AF10 knock-out cells, re-expression wild-type AF10, but not a DOT1L binding-impaired mutant, rescues overall H3K79 methylation and reduces reprogramming efficiency. Transcriptomic analyses during reprogramming show that AF10 suppression results in downregulation of fibroblast-specific genes and accelerates the activation of pluripotency-associated genes.
conclusionsOur findings establish AF10 as a novel barrier to reprogramming by regulating H3K79 methylation and thereby sheds light on the mechanism by which cell identity is maintained in somatic cells.
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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.