DDX41 haploinsufficiency causes inefficient hematopoiesis under stress and cooperates with p53 mutations to cause hematologic malignancy.


Journal

Leukemia
ISSN: 1476-5551
Titre abrégé: Leukemia
Pays: England
ID NLM: 8704895

Informations de publication

Date de publication:
27 Jun 2024
Historique:
received: 20 11 2023
accepted: 07 06 2024
revised: 05 06 2024
medline: 28 6 2024
pubmed: 28 6 2024
entrez: 27 6 2024
Statut: aheadofprint

Résumé

Germline heterozygous mutations in DDX41 predispose individuals to hematologic malignancies in adulthood. Most of these DDX41 mutations result in a truncated protein, leading to loss of protein function. To investigate the impact of these mutations on hematopoiesis, we generated mice with hematopoietic-specific knockout of one Ddx41 allele. Under normal steady-state conditions, there was minimal effect on lifelong hematopoiesis, resulting in a mild yet persistent reduction in red blood cell counts. However, stress induced by transplantation of the Ddx41

Identifiants

pubmed: 38937548
doi: 10.1038/s41375-024-02304-9
pii: 10.1038/s41375-024-02304-9
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : U.S. Department of Health & Human Services | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (National Institute of Diabetes & Digestive & Kidney Diseases)
ID : K01DK121733
Organisme : U.S. Department of Defense (United States Department of Defense)
ID : W81XWH-22-1-0805

Informations de copyright

© 2024. The Author(s).

Références

Makishima H, Saiki R, Nannya Y, Korotev SC, Gurnari C, Takeda J, et al. Germline DDX41 mutations define a unique subtype of myeloid neoplasms. Blood. 2022;141:534–49.
Li P, Brown S, Williams M, White T, Xie W, Cui W, et al. The genetic landscape of germline DDX41 variants predisposing to myeloid neoplasms. Blood. 2022;140:716–55.
doi: 10.1182/blood.2021015135 pubmed: 35671390 pmcid: 9389629
Choi EJ, Cho YU, Hur EH, Jang S, Kim N, Park HS, et al. Unique ethnic features of DDX41 mutations in patients with idiopathic cytopenia of undetermined significance, myelodysplastic syndrome, or acute myeloid leukemia. Haematologica. 2021;107:510–8.
Sébert M, Passet M, Raimbault A, Rahmé R, Raffoux E, Sicre de Fontbrune F, et al. Germline DDX41 mutations define a significant entity within adult MDS/AML patients. Blood. 2019;134:1441–4.
doi: 10.1182/blood.2019000909 pubmed: 31484648
Quesada AE, Routbort MJ, DiNardo CD, Bueso-Ramos CE, Kanagal-Shamanna R, Khoury JD, et al. DDX41 mutations in myeloid neoplasms are associated with male gender, TP53 mutations and high-risk disease. Am J Hematol. 2019;94:757–66.
doi: 10.1002/ajh.25486 pubmed: 30963592
Polprasert C, Schulze I, Sekeres MA, Makishima H, Przychodzen B, Hosono N, et al. Inherited and Somatic Defects in DDX41 in Myeloid Neoplasms. Cancer Cell. 2015;27:658–70.
doi: 10.1016/j.ccell.2015.03.017 pubmed: 25920683 pmcid: 8713504
Badar T, Chlon T. Germline and somatic defects in ddx41 and its impact on myeloid neoplasms. Curr Hematol Malig Rep. 2022;17:113–20.
Chlon TM, Stepanchick E, Hershberger CE, Daniels NJ, Hueneman KM, Kuenzi Davis A, et al. Germline DDX41 mutations cause ineffective hematopoiesis and myelodysplasia. Cell Stem Cell. 2021;28:1966–81.
Qu S, Li B, Qin T, Xu Z, Pan L, Hu N, et al. Molecular and clinical features of myeloid neoplasms with somatic DDX41 mutations. Br J Haematol. 2020;192:1006–10.
Bataller A, Loghavi S, Gerstein Y, Bazinet A, Sasaki K, Chien KS, et al. Characteristics and clinical outcomes of patients with myeloid malignancies and DDX41 variants. Am J Hematol. 2023;98:1780–90.
Weinreb JT, Bowman TV. Clinical and mechanistic insights into the roles of DDX41 in haematological malignancies. FEBS Lett. 2022;596:2736–45.
doi: 10.1002/1873-3468.14487 pubmed: 36036093 pmcid: 9669125
Jacks T, Remington L, Williams BO, Schmitt EM, Halachmi S, Bronson RT, et al. Tumor spectrum analysis in p53-mutant mice. Curr Biol. 1994;4:1–7.
doi: 10.1016/S0960-9822(00)00002-6 pubmed: 7922305
Hidalgo San Jose L, Signer RAJ. Cell-type-specific quantification of protein synthesis in vivo. Nat Protoc. 2019;14:441–60.
doi: 10.1038/s41596-018-0100-z pubmed: 30610239
Shuga J, Zhang J, Samson LD, Lodish HF, Griffith LG. In vitro erythropoiesis from bone marrow-derived progenitors provides a physiological assay for toxic and mutagenic compounds. Proc Natl Acad Sci. 2007;104:8737–42.
doi: 10.1073/pnas.0701829104 pubmed: 17502613 pmcid: 1885572
Choi K, Ratner N. iGEAK: an interactive gene expression analysis kit for seamless workflow using the R/shiny platform. BMC Genomics. 2019;20:177.
doi: 10.1186/s12864-019-5548-x pubmed: 30841853 pmcid: 6404331
Emig D, Salomonis N, Baumbach J, Lengauer T, Conklin BR, Albrecht M. AltAnalyze and DomainGraph: analyzing and visualizing exon expression data. Nucleic Acids Res. 2010;38:W755–762.
doi: 10.1093/nar/gkq405 pubmed: 20513647 pmcid: 2896198
Zheng GXY, Terry JM, Belgrader P, Ryvkin P, Bent ZW, Wilson R, et al. Massively parallel digital transcriptional profiling of single cells. Nat Commun. 2017;8:14049.
doi: 10.1038/ncomms14049 pubmed: 28091601 pmcid: 5241818
Hao Y, Hao S, Andersen-Nissen E, Mauck WM, Zheng S, Butler A, et al. Integrated analysis of multimodal single-cell data. Cell. 2021;184:3573–3587.e3529.
doi: 10.1016/j.cell.2021.04.048 pubmed: 34062119 pmcid: 8238499
Love MI, Huber W, Anders S. Moderated estimation of fold change and dispersion for RNA-seq data with DESeq2. Genome Biol. 2014;15:550.
doi: 10.1186/s13059-014-0550-8 pubmed: 25516281 pmcid: 4302049
Poplin R, Chang P-C, Alexander D, Schwartz S, Colthurst T, Ku A, et al. A universal SNP and small-indel variant caller using deep neural networks. Nat Biotechnol. 2018;36:983–7.
doi: 10.1038/nbt.4235 pubmed: 30247488
Cingolani P, Platts A, Wang le L, Coon M, Nguyen T, Wang L, et al. A program for annotating and predicting the effects of single nucleotide polymorphisms, SnpEff: SNPs in the genome of Drosophila melanogaster strain w1118; iso-2; iso-3. Fly. 2012;6:80–92.
doi: 10.4161/fly.19695 pubmed: 22728672 pmcid: 3679285
Ma J, Mahmud N, Bosland MC, Ross SR. DDX41 is needed for pre- and postnatal hematopoietic stem cell differentiation in mice. Stem Cell Rep. 2022;17:879–93. 2022/04/12/
doi: 10.1016/j.stemcr.2022.02.010
Harris BD, Lee J, Gillis J. A Meta-Analytic Single-Cell Atlas of Mouse Bone Marrow Hematopoietic Development. bioRxiv. 2021. https://www.biorxiv.org/content/10.1101/2021.08.12.456098v1 .
Kuleshov MV, Jones MR, Rouillard AD, Fernandez NF, Duan Q, Wang Z, et al. Enrichr: a comprehensive gene set enrichment analysis web server 2016 update. Nucleic Acids Res. 2016;44:W90–97.
doi: 10.1093/nar/gkw377 pubmed: 27141961 pmcid: 4987924
Dutt S, Narla A, Lin K, Mullally A, Abayasekara N, Megerdichian C, et al. Haploinsufficiency for ribosomal protein genes causes selective activation of p53 in human erythroid progenitor cells. Blood. 2011;117:2567–76.
doi: 10.1182/blood-2010-07-295238 pubmed: 21068437 pmcid: 3062351
Lindstroöm MS, Jin A, Deisenroth C, White Wolf G, Zhang Y. Cancer-Associated Mutations in the MDM2 Zinc Finger Domain Disrupt Ribosomal Protein Interaction and Attenuate MDM2-Induced p53 Degradation. Mol Cell Biol. 2007;27:1056–68.
doi: 10.1128/MCB.01307-06
Kamio T, Gu B-w, Olson TS, Zhang Y, Mason PJ, Bessler M. Mice with a Mutation in the Mdm2 Gene That Interferes with MDM2/Ribosomal Protein Binding Develop a Defect in Erythropoiesis. PLOS ONE. 2016;11:e0152263.
doi: 10.1371/journal.pone.0152263 pubmed: 27042854 pmcid: 4820113
Weinreb JT, Gupta V, Sharvit E, Weil R, Bowman TV. Ddx41 inhibition of DNA damage signaling permits erythroid progenitor expansion in zebrafish. Haematologica. 2022;107:644–54.
doi: 10.3324/haematol.2020.257246 pubmed: 33763998
Weinreb JT, Ghazale N, Pradhan K, Gupta V, Potts KS, Tricomi B, et al. Excessive R-loops trigger an inflammatory cascade leading to increased HSPC production. Dev Cell. 2021;56:627–.e625.
doi: 10.1016/j.devcel.2021.02.006 pubmed: 33651979 pmcid: 8258699
Kadono M, Kanai A, Nagamachi A, Shinriki S, Kawata J, Iwato K, et al. Biological implications of somatic DDX41 p.R525H mutation in acute myeloid leukemia. Exp Hematol. 2016;44:745–.e744.
doi: 10.1016/j.exphem.2016.04.017 pubmed: 27174803
Mosler T, Conte F, Longo GMC, Mikicic I, Kreim N, Möckel MM, et al. R-loop proximity proteomics identifies a role of DDX41 in transcription-associated genomic instability. Nat Commun. 2021;12:7314.
doi: 10.1038/s41467-021-27530-y pubmed: 34916496 pmcid: 8677849
Cheloor Kovilakam S, Gu M, Dunn WG, Marando L, Barcena C, Nik-Zainal S, et al. Prevalence and significance of DDX41 gene variants in the general population. Blood. 2023;142:1185–92.
doi: 10.1182/blood.2023020209 pubmed: 37506341
Barreyro L, Chlon TM, Starczynowski DT. Chronic immune response dysregulation in MDS pathogenesis. Blood. 2018;132:1553–60.
doi: 10.1182/blood-2018-03-784116 pubmed: 30104218 pmcid: 6182269

Auteurs

Emily Stepanchick (E)

Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.

Andrew Wilson (A)

Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.

Analise M Sulentic (AM)

Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.

Kwangmin Choi (K)

Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.

Kathleen Hueneman (K)

Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.

Daniel T Starczynowski (DT)

Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Department of Pediatrics, University of Cincinnati, Cincinnati, OH, USA.
Department of Cancer Biology, University of Cincinnati, Cincinnati, OH, USA.
University of Cincinnati Cancer Center, Cincinnati, OH, USA.

Timothy M Chlon (TM)

Division of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA. Timothy.Chlon@cchmc.org.
Department of Pediatrics, University of Cincinnati, Cincinnati, OH, USA. Timothy.Chlon@cchmc.org.
Department of Cancer Biology, University of Cincinnati, Cincinnati, OH, USA. Timothy.Chlon@cchmc.org.
University of Cincinnati Cancer Center, Cincinnati, OH, USA. Timothy.Chlon@cchmc.org.

Classifications MeSH