ArticleBritish journal of haematology2011
Ribosomal protein L11 mutation in zebrafish leads to haematopoietic and metabolic defects.
Article in British journal of haematology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.
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Who cites it
62 citing papers in PubMed, 92 citations in OpenAlex.
- Article
- Article
- General transcription factor IIIAa regulates the transcription of somatic 5S rRNA and influences embryonic organ development in zebrafish.Marine life science & technology · 2026Article
- Ribosomal biogenesis defects trigger subunit specific developmental checkpoints via TOR signaling and gap junction in C. elegans.Developmental biology · 2026Article
- Ribosome specialization by cancer-associated ribosomal protein mutations: progress made and open questions.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025Review
- Article
- mTORC1 mediates the expansion of hematopoietic stem and progenitor cells through ribosome biogenesis protein Urb2 in zebrafish.Stem cell reports · 2024Article
- An atypical form of 60S ribosomal subunit in Diamond-Blackfan anemia linked to RPL17 variants.JCI insight · 2024Article
- Animal models of Diamond-Blackfan anemia: updates and challenges.Haematologica · 2023Review
- Nucleolar Protein 56 Deficiency in Zebrafish Leads to Developmental Abnormalities and Anemia viaBiology · 2023Article
- Identifying ribosome heterogeneity using ribosome profiling.Nucleic acids research · 2022Article
- Downregulation of SATB1 by miRNAs reduces megakaryocyte/erythroid progenitor expansion in preclinical models of Diamond-Blackfan anemia.Experimental hematology · 2022Article
- Cell autonomous and non-autonomous consequences of deviations in translation machinery on organism growth and the connecting signalling pathways.Open biology · 2022Review
- Ddx41 inhibition of DNA damage signaling permits erythroid progenitor expansion in zebrafish.Haematologica · 2022Article
- The Ribosome Biogenesis Factor Ltv1 Is Essential for Digestive Organ Development and Definitive Hematopoiesis in Zebrafish.Frontiers in cell and developmental biology · 2021Article
- Oxidative DNA Damage, Inflammatory Signature, and Altered Erythrocytes Properties in Diamond-Blackfan Anemia.International journal of molecular sciences · 2020Article
- Calmodulin inhibitors improve erythropoiesis in Diamond-Blackfan anemia.Science translational medicine · 2020Article
- Pseudouridylation defect due toProceedings of the National Academy of Sciences of the United States of America · 2020Article
- Hallmarks of ribosomopathies.Nucleic acids research · 2020Review
- Loss ofG3 (Bethesda, Md.) · 2019Article
2 more citing papers are in PubMed but not listed here.
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3 authors at 2 institutions in 2 countries.
Funding
Abstract
Mutations in ribosomal proteins are associated with a congenital syndrome, Diamond-Blackfan anaemia (DBA), manifested by red blood cell aplasia, developmental abnormalities and increased risk of malignancy. Recent studies suggest the involvement of p53 activation in DBA. However, which pathways are involved and how they contribute to the DBA phenotype remains unknown. Here we show that a zebrafish mutant for the rpl11 gene had defects both in the development of haematopoietic stem cells (HSCs) and maintenance of erythroid cells. The molecular signature of the mutant included upregulation of p53 target genes and global changes in metabolism. The changes in several pathways may affect haematopoiesis including upregulation of pro-apoptotic and cell cycle arrest genes, suppression of glycolysis, downregulation of biosynthesis and dysregulation of cytoskeleton. Each of these pathways has been individually implicated in haematological diseases. Inhibition of p53 partially rescued haematopoiesis in the mutant. Altogether, we propose that the unique phenotype of DBA is a sum of several abnormally regulated molecular pathways, mediated by the p53 protein family and p53-independent, which have synergistic impact on haematological and other cellular pathways affected in DBA. Our results provide new insights into the pathogenesis of DBA and point to the potential avenues for therapeutic intervention.
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