ArticleNature communications2025
DDX41 resolves G-quadruplexes to maintain erythroid genome integrity and prevent cGAS-mediated cell death.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- G-Quadruplexes: Structural Diversity and Emerging Roles in Biomolecular Condensation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Review
- [Germline DDX41 mutations and myelodysplastic neoplasms].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2026Review
- Spatial transcriptomic analyses highlight distinct erythroid niches in mice and humans.Nature genetics · 2026Article
- Stromal Gasdermin D-mediated Pyroptosis Drives Maladaptive CD4bioRxiv : the preprint server for biology · 2026Article
- MDS/AML-associated DDX41 helicase facilitates homologous recombination repair by potentially resolving R-loops.Nucleic acids research · 2026Article
- Targeting R-loops: diverse RNA helicases in R-loop resolution and their potential as targets for cancer therapy.Frontiers in cell and developmental biology · 2026Review
- Oncogenic DEAD-box ATPase DDX41 establishes transcript ensembles via CLK3-dependent and -independent mechanisms.Nature communications · 2025Article
- The CGG triplet repeat binding protein 1 counteracts R-loop induced transcription-replication stress.EMBO reports · 2025Article
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Abstract
Deleterious germline DDX41 variants constitute the most common inherited predisposition disorder linked to myeloid neoplasms (MNs), yet their role in MNs remains unclear. Here we show that DDX41 is essential for erythropoiesis but dispensable for other hematopoietic lineages. Ddx41 knockout in early erythropoiesis is embryonically lethal, while knockout in late-stage terminal erythropoiesis allows mice to survive with normal blood counts. DDX41 deficiency induces a significant upregulation of G-quadruplexes (G4), which co-distribute with DDX41 on the erythroid genome. DDX41 directly binds to and resolves G4, which is significantly compromised in MN-associated DDX41 mutants. G4 accumulation induces erythroid genome instability, ribosomal defects, and p53 upregulation. However, p53 deficiency does not rescue the embryonic death of Ddx41 hematopoietic-specific knockout mice. In parallel, genome instability also activates the cGas-Sting pathway, impairing survival, as cGas deficiency rescues the lethality of hematopoietic-specific Ddx41 knockout mice. This is supported by data from a DDX41-mutated MN patient and human iPSC-derived bone marrow organoids. Our study establishes DDX41 as a G4 resolvase, essential for erythroid genome stability and suppressing the cGAS-STING pathway.
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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 Socratic graph.