Expression data from zebrafish depleted of Esco2
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ABSTRACT:
ORGANISM(S): Danio rerio
PROVIDER: GSE27569 | GEO | 2011/03/01
SECONDARY ACCESSION(S): PRJNA138409
REPOSITORIES: GEO
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Project description:Our study in zebrafish is the first to use an animal model to understand the biology of the developmental disorder Roberts Syndrome (RBS). RBS is caused by mutations in the ESCO2 gene. We have used morpholinos (MO) to knock down esco2 in zebrafish to better understand the pathology of this rare human syndrome. Our zebrafish model nicely phenocopies the developmental defects observed in RBS. RNA from esco2 morphants and control (injected with buffer only) zebrafish embryos collected at 24 hours post-fertilization (h.p.f.) and 48 h.p.f. was hybridized to Affymetrix microarrays (Gene Chip zebrafish genome arrays cat. no. 900488). Four pools of 50 embryos for each genotype and time point were used as the RNA source, and RNA from each pool was hybridized independently such that the experiment had four biological replicates. Note that the chip for the 2nd replicate of the control embryos at 48 h.p.f. was faulty and the data is therefore not included.
2011-03-01 | E-GEOD-27569 | biostudies-arrayexpress
Project description:Roberts syndrome (RBS) is a human developmental disorder caused by mutations in the cohesin acetyltransferase ESCO2. We previously reported that mTORC1 was inhibited and overall translation was reduced in RBS cells. Treatment of RBS cells with L-leucine partially rescued mTOR function and protein synthesis, correlating with increased cell division. In this study, we use RBS as a model for mTOR inhibition and analyze transcription and translation with ribosome profiling to determine genome-wide effects of L-leucine. The translational efficiency of many genes is increased with Lleucine in RBS cells including genes involved in ribosome biogenesis, translation, and mitochondrial function. snoRNAs are strongly upregulated in RBS cells, but decreased with L-leucine. Imprinted genes, including H19 and GTL2, are differentially expressed in RBS cells consistent with contribution to mTORC1 control. This study reveals dramatic effects of L-leucine stimulation of mTORC1 and supports that ESCO2 function is required for normal gene expression and translation. 42 samples of human fibroblast cell lines with various genotypes (wt, corrected, and esco2 mutants) are treated with l-leucine or d-leucine (control) for 3 or 24 hours. Biological replicates are present.
2016-01-15 | E-GEOD-64962 | biostudies-arrayexpress
Project description:Roberts syndrome (RBS) is a human developmental disorder caused by mutations in the cohesin acetyltransferase ESCO2. We previously reported that mTORC1 was inhibited and overall translation was reduced in RBS cells. Treatment of RBS cells with L-leucine partially rescued mTOR function and protein synthesis, correlating with increased cell division. In this study, we use RBS as a model for mTOR inhibition and analyze transcription and translation with ribosome profiling to determine genome-wide effects of L-leucine. The translational efficiency of many genes is increased with Lleucine in RBS cells including genes involved in ribosome biogenesis, translation, and mitochondrial function. snoRNAs are strongly upregulated in RBS cells, but decreased with L-leucine. Imprinted genes, including H19 and GTL2, are differentially expressed in RBS cells consistent with contribution to mTORC1 control. This study reveals dramatic effects of L-leucine stimulation of mTORC1 and supports that ESCO2 function is required for normal gene expression and translation.
2016-01-15 | GSE64962 | GEO
Project description:TÜAB zebrafish were maintained at 28.5 °C in in 1x Danieau solution (58 mM NaCl, 0.7 mM KCl, 0.4 mM MgSO4, 0.6 mM Ca (NO3)2, 5 mM HEPES, pH 7.6, 0.0001 % Methylene blue). Morpholinos (Gene Tools, Philomath, OR) were designed against Danio rerio lin-9 homolog (Genebank accession NM_001044946). The morpholino (MO) sequences were MO-E1 5´-GTTAGTTTTATTACTCACTCTCGTC-3´ and 5-base mismatch morpholino MO-E1mis 5´-GTTACTTTTAATACTGACTGTCCTC-3´. 7 ng of morpholinos were injected into one cell-stage embryos. 20 embryos per condition (MO E1; MO E1mis) were pooled for RNA purification 24 h post fertilization. Using the two color Quick-Amp Labeling Kit (Agilent; 5190-0444) 100 ng of total RNA were used for cDNA synthesis, mRNA amplification and labeling according to manufacturers instructions. Transcriptional profiling was done on a zebrafish oligo array (Agilent; G2519F AMADID 019161) in a 4 x 44K slide format and analyzed as described before.<br>
2009-03-28 | E-MEXP-2100 | biostudies-arrayexpress
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2011-12-17 | E-GEOD-34508 | biostudies-arrayexpress
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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
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
Project description:miRNA profiling of zebrafish embryos comparing control MO with Lin28A MO or Lin28B MO injected embryos at 5hpf
2013-11-19 | GSE52492 | GEO
