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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Transcription profiling of zebrafish embryos injected with DrC1q-like morpholino and control morpholino

ABSTRACT: Except complement C1q, the immunological functions of other C1q family members have remained unclear. In vitro studies showed that DrC1q-like could inhibit the apoptosis induced by ActD and CHX in EPC cells, through repressing the activation of caspase 3/9. Moreover, its physiological roles were studied by morpholino-mediated knockdown in zebrafish embryogenesis; We used microarrays to compare the global programme of gene expression of DrC1q-like deficient embryos and control embryos. And identified distinct classes of up-regulated and down-regulated genes in DrC1q-like deficient embryos. Experiment Overall Design: Zebrafish embryos were selected at 24hpf for RNA extraction and hybridization on Affymetrix microarrays. We sought to obtain expression profiles of DrC1q-like deficient embryos compared to the control. And we could find out which genes and pathways were affected by DrC1q-like

ORGANISM(S): Danio rerio

SUBMITTER: Jie Mei

PROVIDER: E-GEOD-8800 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from embryos injected with DrC1q-like morpholino and control morpholino

Project description:Except complement C1q, the immunological functions of other C1q family members have remained unclear. In vitro studies showed that DrC1q-like could inhibit the apoptosis induced by ActD and CHX in EPC cells, through repressing the activation of caspase 3/9. Moreover, its physiological roles were studied by morpholino-mediated knockdown in zebrafish embryogenesis We used microarrays to compare the global programme of gene expression of DrC1q-like deficient embryos and control embryos. And identified distinct classes of up-regulated and down-regulated genes in DrC1q-like deficient embryos. Keywords: time course

2007-12-29 | GSE8800 | GEO

RNA-seq of HNRNPAB morpholino in zebrafish

Project description:To investigate the transcriptomic alterations following 24hpf knockdown of the gene HNRNPAB in zebrafish, we injected HNRNPAB morpholino with 3ng and 6ng into 1-cell zebrafish embryos separately, and the 24hpf embryos were collected for RNA-seq.

2022-03-31 | GSE199586 | GEO

Transcription profiling of zebrafish neuromasts to investigate the role of ERbeta2 in neuromasts development

Project description:The role of ERbeta2 in zebrafish larvae was investigated by injection of a Morpholino against ERbeta2. After 72hpf, the morphants showed a strong disruption in their sensory systems. ERbeta2 has been shown to be needed for the normal functioning of the sensory system organs, the neuromasts. The mechanisms involved in the neuromast disruption in ERbeta2 morphants was identified by microarrays gene screening. After comparison of two screening with low and high concentration of Morpholinos, genes that were present in the two microarrays screening were selected. The genes were then chosen by relevance for the mechanisms involved in the role of ERbeta2 in neuromast development. The ngn1 transcription factor, Notch3 and Notch1a showed to be up-regulated, also confirmed by in situ hybridization. The Notch signaling is known to be involved in cell fate in developing neuromasts. The overall conclusion is that ERbeta2 by interacting with the notch signaling pathways is critical for normal development of the neuromast of the lateral line in zebrafish. Experiment Overall Design: Zebrafish eggs until 4 cell stage were injected either with Morpholino blocking the translation ERbeta2 (ERbeta2 MO), either with a standard control Morpholino (coMO) at a concentration of 15uM. Two biological replicates for ERbeta2 MO, two replicates for coMO and two replicates for uninjected embryos (blank). A total of 6 samples were performed.

2008-10-26 | E-GEOD-13157 | biostudies-arrayexpress

Transcription profiling of zebrafish embryos to investigate the role of ERbeta2 in zebrafish neuromasts development - 50uM

Project description:The role of ERbeta2 in zebrafish larvae was investigated by injection of a Morpholino against ERbeta2. After 72hpf, the morphants showed a strong disruption in their sensory systems. ERbeta2 has been shown to be needed for the normal functioning of the sensory system organs, the neuromasts. The mechanisms involved in the neuromast disruption in ERbeta2 morphants was identified by microarrays gene screening. After comparison of two screening with low and hign concentration of Morpholinos, genes that were present in the two microarrays screening were selected. The genes were then chosen by relevance for the mechanisms involved in the role of ERbeta2 in neuromast development. The ngn1 transcription factor, Notch3 and Notch1a showed to be up-regulated, also confirmed by in situ hybridization. The Notch signaling is known to be involved in cell fate in developing neuromasts. The overall conclusion is that ERbeta2 by interacting with the notch signaling pathways is critical for normal development of the neuromast of the lateral line in zebrafish. Experiment Overall Design: Zebrafish eggs until 4 cell stage were injected either with Morpholino blocking the translation ERbeta2 (ERbeta2 MO), either with a standard control Morpholino (coMO) at a concentration of 50uM. Two biological replicates for ERbeta2 MO, two replicates for coMO and two replicates for uninjected embryos (blank). A total of 6 samples were performed.

2008-10-26 | E-GEOD-13158 | biostudies-arrayexpress

Assessment of hematopoietic failure due to RPL11 deficiency in a zebrafish model of DiamondM-bM-^@M-^SBlackfan anemia by deep sequencing

Project description:To comprehensively reflect the impact of RPL11 deficiency on the transcriptome of zebrafish embryos, we collected 40M-bM-^@M-^S50 RPL11-deficient and MO control zebrafish embryos at 48 hpf from separate experiments and constructed two mRNA-seq sequencing libraries in parallel. High-throughput sequencing was performed on the Hi-Seq2000 sequencing platform in parallel. The number of sequenced gene transcript reads was 35M-bM-^@M-^S40 million. We found that hemoglobin biosynthetic and hematological defects in RPL11-deficient zebrafish were related to dysregulation of iron metabolism-related genes, including tfa, tfr1b, alas2 and slc25a37, which are involved in heme and hemoglobin biosynthesis. In addition, we found reduced expression of the hematopoietic stem cells (HSC) marker c-myb and HSC transcription factor tal1 and hoxb4a in RPL11-deficient zebrafish embryos, indicating that the hematopoietic defects may be related to impaired HSC differentiation and proliferation. However, RPL11 deficiency did not affect the development of other blood cell lineages such as granulocytes and myelocytes. Compare 2 different transcriptomes of RPL11-deficient and MO control zebrafish embryos

2014-01-21 | E-GEOD-51326 | biostudies-arrayexpress

Transcription profiling of trf3 morpholino treated zebrafish embryos to identify Trf3 target genes

Project description:To identify Trf3 target genes, we performed expression profiling in trf3 MO-treated embryos (at 6 hpf) using a zebrafish oligonucleotide microarray representing ~12,800 genes.

2007-10-29 | E-MEXP-1279 | biostudies-arrayexpress

Proprotein Convertase Subtilisin/Kexin Type 7 (PCSK7) Is Essential for the Zebrafish Development and Bioavailability of Transforming Growth Factor Î²1a (TGFÎ²1a)

Project description:Proprotein convertase subtilisin/kexin (PCSK) enzymes convert proproteins into bioactive end products. Although other PCSK enzymes are known to be essential for biological processes ranging from cholesterol metabolism to host defense, the in vivo importance of the evolutionarily ancient PCSK7 has remained enigmatic. Here, we quantified the expressions of all pcsk genes during the 1st week of fish development and in several tissues. pcsk7 expression was ubiquitous and evident already during the early development. To compare mammalian and zebrafish PCSK7, we prepared homology models, which demonstrated remarkable structural conservation. When the PCSK7 function in developing larvae was inhibited, we found that PCSK7-deficient fish have defects in various organs, including the brain, eye, and otic vesicle, and these result in mortality within 7 days postfertilization. A genome-wide analysis of PCSK7-dependent gene expression showed that, in addition to developmental processes, several immune system-related pathways are also regulated by PCSK7. Specifically, the PCSK7 contributed to the mRNA expression and proteolytic cleavage of the cytokine TGFÎ²1a. Consequently, tgfÎ²1a morphant fish displayed phenotypical similarities with pcsk7 morphants, underscoring the importance of this cytokine in the zebrafish development. Targeting PCSK activity has emerged as a strategy for treating human diseases. Our results suggest that inhibiting PCSK7 might interfere with normal vertebrate development. Gene expressions of zebrafish were measured at 6 and 24 hours post fertilization of the fish samples with PCSK7 blocked with morpholino technology. For each time point, triplicate samples pooled from 18-35 zebrafish embryos were used. Also gene expressions from triplicate control samples were measured.

2014-01-02 | E-GEOD-42070 | biostudies-arrayexpress

Transcription profiling of mouse how germ-line clones embryos and WT embryos at 3-5 h AEL

Project description:Mutant embryos lacking maternal and zygotic HOW exhibit defects in mesoderm development. How is an RNA binding protein that regulates the levels of mRNAs by controling RNA metabolism. To gain an insight as to the profile of mRNAs regulated by HOW during early mesoderm development we analyzed the array of mRNAs whose levels are altered in the how mutant embryos. Experiment Overall Design: Embryos lacking both maternal and zygoic HOW were selected using a GFP balancer. The mRNA of 5 collections of 3-5 hrs old WT or how mutant embryos were pooled and used for each microarray experiment. Two microarray experiments were performed from independent samples.

2008-06-15 | E-GEOD-7772 | biostudies-arrayexpress

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

Project description: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

2015-05-18 | E-GEOD-54152 | biostudies-arrayexpress

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

Project description: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 miRNome between RPS24-deficient and MO control zebrafish embryos for understanding the complex molecular pathogenesis of mutant RPS24-mediated human diseases

2015-05-18 | E-GEOD-54259 | biostudies-arrayexpress

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