ArticleHaematologica2022
ZRSR1 co-operates with ZRSR2 in regulating splicing of U12-type introns in murine hematopoietic cells.
Article in Haematologica, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Dysregulation of U12-Type Splicing in Lupus Neutrophils.Arthritis & rheumatology (Hoboken, N.J.) · 2026Article
- Dysregulation of U12-Type Splicing in Lupus Neutrophils.bioRxiv : the preprint server for biology · 2025Article
- Acute myeloid leukemia with plasmacytoid dendritic cell proliferation: A case report and literature review.Oncology letters · 2025Article
- Comprehensive analysis of the clinical feature, myeloid neoplasm-related gene mutation profiles and T cell diversity acquired pure red cell aplasia.Annals of hematology · 2025Article
- ZRSR2 loss causes aberrant splicing in JAK2HemaSphere · 2025Article
- Disrupted minor intron splicing activates reductive carboxylation-mediated lipogenesis to drive metabolic dysfunction-associated steatotic liver disease progression.The Journal of clinical investigation · 2025Article
- Connecting genotype and phenotype in minor spliceosome diseases.RNA (New York, N.Y.) · 2025Review
- Possible new mechanisms of primary drug resistance in NSCLC with EGFR mutation treated with Osimertinib.IUBMB life · 2025Article
- The emerging significance of splicing in vertebrate development.Development (Cambridge, England) · 2022Review
- Zrsr2 Is Essential for the Embryonic Development and Splicing of Minor Introns in RNA and Protein Processing Genes in Zebrafish.International journal of molecular sciences · 2022Article
- Dysregulated minor intron splicing in cancer.Cancer science · 2022Review
- Molecular Threat of Splicing Factor Mutations to Myeloid Malignancies and Potential Therapeutic Modulations.Biomedicines · 2022Review
- Comprehensive analysis of spliceosome genes and their mutants across 27 cancer types in 9070 patients: clinically relevant outcomes in the context of 3P medicine.The EPMA journal · 2022Article
- Article
- Sex-BiasedCancer discovery · 2022Article
- Review
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Authors and funding
16 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recurrent loss-of-function mutations of spliceosome gene, ZRSR2, occur in myelodysplastic syndromes (MDS). Mutation/loss of ZRSR2 in human myeloid cells primarily causes impaired splicing of the U12-type introns. In order to further investigate the role of this splice factor in RNA splicing and hematopoietic development, we generated mice lacking ZRSR2. Unexpectedly, Zrsr2-deficient mice developed normal hematopoiesis with no abnormalities in myeloid differentiation evident in either young or ≥1-year old knockout mice. Repopulation ability of Zrsr2-deficient hematopoietic stem cells was also unaffected in both competitive and non-competitive reconstitution assays. Myeloid progenitors lacking ZRSR2 exhibited mis-splicing of U12-type introns, however, this phenotype was moderate compared to the ZRSR2-deficient human cells. Our investigations revealed that a closely related homolog, Zrsr1, expressed in the murine hematopoietic cells, but not in human cells contributes to splicing of U12-type introns. Depletion of Zrsr1 in Zrsr2 KO myeloid cells exacerbated retention of the U12-type introns, thus highlighting a collective role of ZRSR1 and ZRSR2 in murine U12-spliceosome. We also demonstrate that aberrant retention of U12-type introns of MAPK9 and MAPK14 leads to their reduced protein expression. Overall, our findings highlight that both ZRSR1 and ZRSR2 are functional components of the murine U12-spliceosome, and depletion of both proteins is required to accurately model ZRSR2-mutant MDS in mice.
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