ArticleMolecular cell2021
SALL4 controls cell fate in response to DNA base composition.
Article in Molecular cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 51 citations in OpenAlex.
- Orbital malignant rhabdoid tumor with an aberrant immunophenotype: a case report.Discover oncology · 2026Article
- TCA cycle rewiring underpins histone acetylation sourcing and cell-fate transitions during exit from naive pluripotency.Cell stem cell · 2026Article
- Article
- Neural crest induction requires SALL4-mediated BAF recruitment to lineage specific enhancers.Development (Cambridge, England) · 2025Article
- Zebrafish sall1a and sall4 contribute to body elongation.Developmental biology · 2025Article
- ADT increases prostate cancer cell invasion via altering AR/SALL4/SOX2-OCT4 stem cell signaling.Cell biology and toxicology · 2025Article
- A function of Spalt proteins in heterochromatin organization and maintenance of genomic DNA integrity.Development (Cambridge, England) · 2025Article
- Thalidomide-induced limb malformations: an update and reevaluation.Archives of toxicology · 2025Review
- Reconstitution of pluripotency from mouse fibroblast through Sall4 overexpression.Nature communications · 2024Article
- SALL2 regulates neural differentiation of mouse embryonic stem cells through Tuba1a.Cell death & disease · 2024Article
- Selection on synonymous sites: the unwanted transcript hypothesis.Nature reviews. Genetics · 2024Review
- MeCP2 binds to methylated DNA independently of phase separation and heterochromatin organisation.Nature communications · 2024Article
- Sall genes regulate hindlimb initiation in mouse embryos.Genetics · 2024Article
- Sall4 regulates posterior trunk mesoderm development by promoting mesodermal gene expression and repressing neural genes in the mesoderm.Development (Cambridge, England) · 2024Article
- SALL4 is a CRL3Cell death and differentiation · 2024Article
- Pioneer and PRDM transcription factors coordinate bivalent epigenetic states to safeguard cell fate.Molecular cell · 2024Article
- Sall4 restricts glycolytic metabolism in limb buds through transcriptional regulation of glycolytic enzyme genes.Developmental biology · 2023Article
- Dissecting the roles of MBD2 isoforms and domains in regulating NuRD complex function during cellular differentiation.Nature communications · 2023Article
- The NuRD complex cooperates with SALL4 to orchestrate reprogramming.Nature communications · 2023Article
- Structure of SALL4 zinc finger domain reveals link between AT-rich DNA binding and Okihiro syndrome.Life science alliance · 2023Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
Abstract
Mammalian genomes contain long domains with distinct average compositions of A/T versus G/C base pairs. In a screen for proteins that might interpret base composition by binding to AT-rich motifs, we identified the stem cell factor SALL4, which contains multiple zinc fingers. Mutation of the domain responsible for AT binding drastically reduced SALL4 genome occupancy and prematurely upregulated genes in proportion to their AT content. Inactivation of this single AT-binding zinc-finger cluster mimicked defects seen in Sall4 null cells, including precocious differentiation of embryonic stem cells (ESCs) and embryonic lethality in mice. In contrast, deletion of two other zinc-finger clusters was phenotypically neutral. Our data indicate that loss of pluripotency is triggered by downregulation of SALL4, leading to de-repression of a set of AT-rich genes that promotes neuronal differentiation. We conclude that base composition is not merely a passive byproduct of genome evolution and constitutes a signal that aids control of cell fate.
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Registered trials
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