Project description:Phenotypic characterisation of our zebrafish sfpq homozygous mutants revealed a restricted set of specific defects, unexpected for a protein expressed ubiquitously and involved in such general mechanisms. The CNS was prominently affected, showing brain boundary and axonal defects associated with absence of motility. To investigate a possible specificity in SFPQ functional targets by microarray RNA profiling analysis, comparing the transcriptome of the sfpq homozygous mutants with its wild type and heterozygous siblings at the earliest stage at which the phenotype is robustly recognizable.
Project description:In this dataset we performed RNA-seq on pools of livers dissected at 120 hpf from dnmt1(s904) mutants and phenotipically wild-type looking siblings.
Project description:Transcriptional profiling of zebrafish embryo comparing wild type untreated embryos with embryos injected with morpholino of zf-grna. This assay is used for determination of expression profiling of trunk muscle at 16, 24, 48, 72 hpf under GRN-A deficiency.
Project description:To further characterize the roles of cortisol signaling via the glucocorticoid receptor (GR) in developing zebrafish, we have used morpholino oligonucleotides to knockdown GR protein translation and measured gene expression in RNA extracted from 24 and 36 hours post fertilization (hpf) embryos. The GR morpholino was characterized previously in Nesan et al., 2012, Endocrinology 181, 35-44)
Project description:To further characterize the roles of cortisol signaling via the glucocorticoid receptor (GR) in developing zebrafish, we have used morpholino oligonucleotides to knockdown GR protein translation and measured gene expression in RNA extracted from 24 and 36 hours post fertilization (hpf) embryos. The GR morpholino was characterized previously in Nesan et al., 2012, Endocrinology 181, 35-44) Single-cell zebrafish embryos were microinjected with either active morpholino or mispair control. Embryos were frozen at 24 and 36 hpf and total RNA extracted for microarray analysis. Three independent replicates (different breeding events on separate days) were performed for each treatment per timepoint.
Project description:Adducin 1 (Add1) functions primarily as a membrane cytoskeletal protein, whereas Add1 contains a bipartite nuclear localization signal, implying its special nuclear function. However, the nuclear functional roles of Add1 apart from maintaining cytoskeletal stability remain unknown. Here, we created add1-deficient zebrafish using Tol2 transposon-mediated gene trapping and evaluated how add1 deficiency affected early hematopoiesis development. When add1 is lacking in zebrafish, both the primitive erythropoiesis and definitive hematopoiesis are compromised, and the primitive erythroblast cells are unable to develop into healthy erythrocytes. More significantly, the RNA sequencing results demonstrated that the p53 pathway is activated in the add1-depletion erythroblast cells, causing the erythroblasts to undergo apoptosis at the 14-somites stage and 24 hpf. Additionally, the anemic phenotype and apoptosis in add1-deficient embryos can be partially rescued by p53 insufficiency. Taken together, our findings show that add1 is critical for zebrafish erythropoiesis partially through the p53-mediated apoptotic pathway, which expands the regulatory role of Add1 for nuclear function.