2. Academic Validation
  3. Loss of splicing factor RBM25 promotes the collapse of murine hematopoiesis

Loss of splicing factor RBM25 promotes the collapse of murine hematopoiesis

  • Exp Cell Res. 2026 May 1;458(1):114982. doi: 10.1016/j.yexcr.2026.114982.
Mafalda Araújo Pereira 1,  Mikkel Bruhn Schuster 1,  Marta Tapia 1,  Pedro Aragon-Fernandez 2,  Erwin M Schoof 2,  Bo Torben Porse 3
Affiliations

Affiliations

  • 1 The Finsen Laboratory, Copenhagen University Hospital - Rigshospitalet, Ole Maaløes Vej 5, Copenhagen-N, 2200, Denmark; Biotech Research and Innovation Center (BRIC), University of Copenhagen, Ole Maaløes Vej 5, Copenhagen-N, 2200, Denmark.
  • 2 Department of Biotechnology and Biomedicine, Technical University of Denmark, Søltofts Plads, Kgs.Lyngby, 2800, Denmark.
  • 3 The Finsen Laboratory, Copenhagen University Hospital - Rigshospitalet, Ole Maaløes Vej 5, Copenhagen-N, 2200, Denmark; Biotech Research and Innovation Center (BRIC), University of Copenhagen, Ole Maaløes Vej 5, Copenhagen-N, 2200, Denmark; Department of Clinical Medicine, University of Copenhagen, Blegdamsvej 3B, Copenhagen N, 2200, Denmark. Electronic address: [email protected].
PMID: 41819468 DOI: 10.1016/j.yexcr.2026.114982
Abstract

Whilst pre-mRNA splicing has been demonstrated to play functional roles in normal hematopoiesis, the potential importance of many splicing regulators remains unexplored. RNA-binding motif protein 25, (RBM25), is a splicing factor involved in multiple cellular functions, such as proliferation and Apoptosis, in various tissues as well as in leukemia. Here, we use a conditional knock-out model to show that the fundamental role of RBM25 in alternative splicing is reflected in the pivotal role of the protein for multiple hematopoietic lineages, including long-term hematopoietic stem cells, as well as embryonic stem cells derived from gene targeted mice. In contrast, mono-allelic deletion of Rbm25 did not impair HSC self-renewal or differentiation, neither under steady-state conditions nor after proliferative stress induced by bone marrow transplantation. Thus, we demonstrate that Rbm25 is haplosufficient and required for the maintenance of normal murine hematopoiesis.

Keywords

Hematopoiesis; RBM25; Splicing.

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