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.
Project description:Transcriptional profiling of zebrafish embryos comparing wild type untreated embryos with embryos injected with morpholino of zf-grna. This assay is used for the determination of expression profiling at 22 hpf under GRN-A deficiency.
Project description:Transcriptional profiling of zebrafish embryos comparing wild type untreated embryos with embryos injected with morpholino of zf-grna. This assay is used for the determination of expression profiling at 22 hpf under GRN-A deficiency. Two-condition experiment: wild type vs. MO-grnA treated cells. 3 biological replicates: each group contains 200 embryos.
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:In this study, we performed RNA-seq on 5 dpf livers of uhrf1-hi272 mutants and phenotypically wild-type siblings collected at 120 hpf.
Project description:We used high throughput sequencing to identify differential expression in siblings, hhex mutants and hhex-overexpression endothelial cells at 48 hpf.