ArticleNature cell biology2020
Pro-neuronal activity of Myod1 due to promiscuous binding to neuronal genes.
Article in Nature cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- Combinatorial and Inducible CRISPRa/i Enables Canalized hiPSC Forward Programming and Iterative RefinementbioRxiv : the preprint server for biology · 2026Article
- Combinatorial transcription factor interactions drive modular gene regulatory networks.bioRxiv : the preprint server for biology · 2026Article
- MYOD represses gene expression from non-E-box motifs.Genes & development · 2025Article
- Chromatin-dependent motif syntax defines differentiation trajectories.Molecular cell · 2025Article
- Review
- Cell fate acquisition and reprogramming by the proneural transcription factor ASCL1.Open biology · 2025Review
- Active repression of cell fate plasticity by PROX1 safeguards hepatocyte identity and prevents liver tumorigenesis.Nature genetics · 2025Article
- Recruitment of homodimeric proneural factors by conserved CAT-CAT E-boxes drives major epigenetic reconfiguration in cortical neurogenesis.Nucleic acids research · 2024Article
- APOBEC2 safeguards skeletal muscle cell fate through binding chromatin and regulating transcription of non-muscle genes during myoblast differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Generation of human excitatory forebrain neurons by cooperative binding of proneural NGN2 and homeobox factor EMX1.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Canalizing cell fate by transcriptional repression.Molecular systems biology · 2024Review
- Article
- Next-generation direct reprogramming.Frontiers in cell and developmental biology · 2024Review
- Insights and applications of direct neuronal reprogramming.Current opinion in genetics & development · 2023Review
- Ascl1 and Ngn2 convert mouse embryonic stem cells to neurons via functionally distinct paths.Nature communications · 2023Article
- Transgene-free direct conversion of murine fibroblasts into functional muscle stem cells.NPJ Regenerative medicine · 2023Article
- MYT1L haploinsufficiency in human neurons and mice causes autism-associated phenotypes that can be reversed by genetic and pharmacologic intervention.Molecular psychiatry · 2023Article
- Muscle cell-type diversification is driven by bHLH transcription factor expansion and extensive effector gene duplications.Nature communications · 2023Article
- Deciphering the multi-scale, quantitative cis-regulatory code.Molecular cell · 2023Review
- Tip60-mediated H2A.Z acetylation promotes neuronal fate specification and bivalent gene activation.Molecular cell · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors at 4 institutions in 4 countries.
Funding
Abstract
The on-target pioneer factors Ascl1 and Myod1 are sequence-related but induce two developmentally unrelated lineages-that is, neuronal and muscle identities, respectively. It is unclear how these two basic helix-loop-helix (bHLH) factors mediate such fundamentally different outcomes. The chromatin binding of Ascl1 and Myod1 was surprisingly similar in fibroblasts, yet their transcriptional outputs were drastically different. We found that quantitative binding differences explained differential chromatin remodelling and gene activation. Although strong Ascl1 binding was exclusively associated with bHLH motifs, strong Myod1-binding sites were co-enriched with non-bHLH motifs, possibly explaining why Ascl1 is less context dependent. Finally, we observed that promiscuous binding of Myod1 to neuronal targets results in neuronal reprogramming when the muscle program is inhibited by Myt1l. Our findings suggest that chromatin access of on-target pioneer factors is primarily driven by the protein-DNA interaction, unlike ordinary context-dependent transcription factors, and that promiscuous transcription factor binding requires specific silencing mechanisms to ensure lineage fidelity.
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What OpenQuestion holds
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.