ArticleBMC genomics2014
Systematic transcriptome analysis of the zebrafish model of diamond-blackfan anemia induced by RPS24 deficiency.
Article in BMC genomics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- An atypical form of 60S ribosomal subunit in Diamond-Blackfan anemia linked to RPL17 variants.JCI insight · 2024Article
- Rcl1 depletion impairs 18S pre-rRNA processing at the A1-site and up-regulates a cohort of ribosome biogenesis genes in zebrafish.Nucleic acids research · 2021Article
- The global gene expression outline of the bovine blastocyst: reflector of environmental conditions and predictor of developmental capacity.BMC genomics · 2021Article
- Modeling hematopoietic disorders in zebrafish.Disease models & mechanisms · 2019Review
- Selenoprotein H is an essential regulator of redox homeostasis that cooperates with p53 in development and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Transcriptome analysis reveals a ribosome constituents disorder involved in the RPL5 downregulated zebrafish model of Diamond-Blackfan anemia.BMC medical genomics · 2016Article
- The Ribosome Biogenesis Protein Nol9 Is Essential for Definitive Hematopoiesis and Pancreas Morphogenesis in Zebrafish.PLoS genetics · 2015Article
- Zebrafish Craniofacial Development: A Window into Early Patterning.Current topics in developmental biology · 2015Review
- Direct regulation of p53 by miR-142a-3p mediates the survival of hematopoietic stem and progenitor cells in zebrafish.Cell discovery · 2015Article
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Authors and funding
12 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDiamond-Blackfan anemia (DBA) is a class of human diseases linked to defective ribosome biogenesis that results in clinical phenotypes. Genetic mutations in ribosome protein (RP) genes lead to DBA phenotypes, including hematopoietic defects and physical deformities. However, little is known about the global regulatory network as well as key miRNAs and gene pathways in the zebrafish model of DBA.
resultsIn this study, we establish the DBA model in zebrafish using an RPS24 morpholino and found that RPS24 is required for both primitive hematopoiesis and definitive hematopoiesis processes that are partially mediated by the p53 pathway. Several deregulated genes and miRNAs were found to be related to hematopoiesis, vascular development and apoptosis in RPS24-deficient zebrafish via RNA-seq and miRNA-seq data analysis, and a comprehensive regulatory network was first constructed to identify the mechanisms of key miRNAs and gene pathways in the model. Interestingly, we found that the central node genes in the network were almost all targeted by significantly deregulated miRNAs. Furthermore, the enforced expression of miR-142-3p, a uniquely expressed miRNA, causes a significant decrease in primitive erythrocyte progenitor cells and HSCs.
conclusionsThe present analyses demonstrate that the comprehensive regulatory network we constructed is useful for the functional prediction of new and important miRNAs in DBA and will provide insights into the pathogenesis of mutant rps24-mediated human DBA disease.
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