Transcriptomics

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Systematic Transcriptome Analysis of Zebrafish Model of Diamond-Blackfan Anemia from RPS24 Deficiency (mRNA-Seq)


ABSTRACT: In this study, we found RPS24 is required for both the primitive hematopoiesis and definitive hematopoiesis process partly mediated by P53 pathway. With the RNA-seq and miRNA-seq technique, several deregulated genes and miRNAs were found to be related with hematopoiesis, vascular development and apoptosis process in RPS24-deficient zebrafish. Meanwhile, a comprehensive regulatory network was firstly constructed to indentify the mechanisms of key miRNAs and gene pathways in this Model of Diamond-Blackfan Anemia. Interestingly, we found that the central nodes genes in the network were almost all targeted by significantly deregulated miRNAs, with partial verification from previous studies, revealing that our network-based approach is promising for the identification of new and important miRNAs in DBA. The present study provided comprehensive potential pathogenic genes and miRNAs data that are associated with RPS24-deficient zebrafish embryos as a model of DBA, which should provide a valuable resource for understanding the complex molecular pathogenesis of mutant RPS24-mediated human diseases. Determine the differences of transcriptome between RPS24-deficient and MO control zebrafish embryos for understanding the complex molecular pathogenesis of mutant RPS24-mediated human diseases

ORGANISM(S): Danio rerio  

SUBMITTER: yadong yang   Xiangdong Fang 

PROVIDER: E-GEOD-54152 | ArrayExpress | 2015-05-18

SECONDARY ACCESSION(S): GSE54152SRP035470PRJNA235310

REPOSITORIES: GEO, ArrayExpress, ENA

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Publications

Systematic transcriptome analysis of the zebrafish model of diamond-blackfan anemia induced by RPS24 deficiency.

Song Binfeng B   Zhang Qian Q   Zhang Zhaojun Z   Wan Yang Y   Jia Qiong Q   Wang Xiaomin X   Zhu Xiaofan X   Leung Anskar Yu-Hung AY   Cheng Tao T   Fang Xiangdong X   Yuan Weiping W   Jia Haibo H  

BMC genomics 20140904


BACKGROUND: Diamond-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. RESULTS: In this study, we establish the DBA model in zebrafish using an RPS24 morpholino  ...[more]

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