Project description:Identification of genes downstream of ndr1 in zebrafish blastulas, and identification of direct targets by reference with Smad2 and Eomesa ChIP-seq data Triplicate control injected samples and triplicate samples of embryos injected with 50pg ndr1 mRNA per embryo. Total RNA prepared from ~200 sphere stage embryos per sample.
Project description:Study of Smad2 and Eomesa genomic binding in zebrafish blastulas, their relationship to eachother and the relaptionship between genomic binding and Ndr1 and Eomesa responsive genes as identified by microarray and RNA-seq. Replicate RNA samples from wild-type and MZeomesa sphere stage embryos
Project description:Identification of Tbx6 genomic binding sites during zebrafish somitogenesis in order to identify Tbx6 targets genes Duplicate anti-myc ChIP samples with associated input for heat shocked Tg(hsp70l:tbx6Myc)v8 embryos, plus single paired anti-myc ChIP and input in wild type embryos - 3x ChIP samples; 3x input samples
Project description:Study of Smad2 and Eomesa genomic binding in zebrafish blastulas, their relationship to eachother and the relaptionship between genomic binding and Ndr1 and Eomesa responsive genes as identified by microarray and RNA-seq. Replicate ChIP samples with associated input for Smad2 and Eomesa - 4x ChIP samples (2 per factor); 2x input samples
Project description:Heart formation requires input from two populations of progenitor cells - the first and second heart fields - that differentiate at distinct times and create different cardiac components. The cardiac outflow tract (OFT) is built through recruitment of late-differentiating, second heart field (SHF) -derived cardiomyocytes to the arterial pole of the heart. Mechanisms responsible for selection of an appropriate number of OFT cells from the SHF remain unclear, although several lines of evidence emphasize the importance of FGF signaling in promoting this process. Here, we examine the impact of inhibition of FGF signaling on cardiac transcription profiles in an effort to identify genes operating downstream of FGF during OFT development. We compared hearts from embryos treated with the FGFR inhibitor SU5402 to the hearts from sibling embryos treated with DMSO. Two replicates were performed.
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.
Project description:This SuperSeries is composed of the following subset Series: GSE26707: Zebrafish 27hpf embryos: hdac1 mutant (hi1618) vs sibling GSE26708: Zebrafish embryos: hdac1 Morphants vs Standard control morphants GSE26709: Zebrafish embryos: hdac1 Morphants vs Standard control morphants at 12, 18 and 27 hpf Refer to individual Series
Project description:The Gata4 transcription factor is essential for normal heart development, but the molecular basis for its function remain poorly understood. We profiled at the whole genome level transcript changes in cardiomyocytes when Gata4 is depleted from zebrafish embryos. Our objective was to elucidate the cardiomyocyte-specific molecular program functioning downstream of Gata4 in order to better understand the role of Gata4 in cardiac morphogenesis. Six samples in total are deposited. Three replicate control samples and three replicate Gata4 morphant samples were analyzed.
Project description:Transcriptional profiling of hdac1 ATG morphant zebrafish embryos in comparison to standard control injected embryos. Embryos where injected at the one cell stage with either a translation blocking morpholino (Hdac1 ATG) or Standard control morpholino (StCo). RNA was extracted at 12, 18 and 27hpf from both sets of embryos and compared with a two-colour hybridisation. Timecourse experiment, hdac1 ATG morphants vs. standard control morphants. Biological replicates: 3
Project description:Heart formation requires the fusion of bilateral cardiomyocyte populations as they move toward the embryonic midline. The bHLH transcription factor Hand2 is essential for cardiac fusion; however, the effector genes that execute this function of Hand2 are unknown. Here, we provide the first evidence for a downstream component of the Hand2 pathway that mediates cardiac morphogenesis. Although hand2 is expressed in cardiomyocytes, mosaic analysis demonstrates that hand2 plays a non-autonomous role in regulating cardiomyocyte movement. Gene expression profiles reveal heightened expression of fibronectin 1 (fn1) in hand2 mutant embryos. Reciprocally, overexpression of hand2 leads to decreased Fibronectin levels. Furthermore, reduction of fn1 function enables rescue of cardiac fusion in hand2 mutants: bilateral cardiomyocyte populations merge and exhibit improved tissue architecture, albeit without major changes in apicobasal polarity. Together, our data provide a novel example of a tissue creating a favorable environment for its morphogenesis: the Hand2 pathway establishes an appropriate environment for cardiac fusion through negative modulation of Fn1 levels. Embryos from three independent hand2 mutant (hanS6 allele) heterozyogous crosses were collected. Examination of Tg(myl7:egfp) expression allow sorting of hand2 mutant embryos from their wild-type siblings.