Effect of depletion of id2b on gene expression during zebrafish heart development
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PROVIDER: PRJNA1256283 | ENA |
REPOSITORIES: ENA
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Project description:Purpose: To investigate other possible phenotype of id2b mutant and the mechanism of how id2b fuctions in heart morphogenesis. Methods: Approximate 1000 hearts dissected from 120 hpf id2b+/+; Tg(myl7:mCherry) and id2b-/-; Tg(myl7:mCherry) embryos were collected for RNA sequencing. Results: Enrichment analysis of DEGs demonstrated that the top-ranked anatomical structures affected by id2b deletion included the heart valve, the compact layer of ventricle, and the atrioventricular canal, id2b inactivation also impacted phenotypes such as cardiac muscle contraction and heart contraction. Conclusions: Zebrafish id2b loss of fuction leads to abnormal heart valve and heart contraction defect. Besides, id2b regulates heart contraction through controlling nrg1 synthesis.
2025-07-11 | GSE295737 | GEO
Project description:Defective zebrafish heart regeneration following depletion of let-7
| PRJNA518758 | ENA
Project description:Transcriptomic profile of zebrafish cardiomyocytes throughout heart development
| PRJNA492280 | ENA
Project description:By using transgenic zebrafish lines Tg(nxk2.5:GFP) (Witzel et al. 2012) and Tg(myl7:EGFP) (D'Amico et al. 2007), we have characterized transcriptomic profile of FACS-isolated CM (GFP+) from developing zebrafish heart at 24, 48 and 72 hpf, corresponding to heart tube formation, chamber formation and differentiation and heart maturation, respectively. GFP- cells were used as a control. We have identified cardiac regulatory networks playing a crucial role in heart morphogenesis. To validate their importance in heart development, we employed zebrafish mutants of cardiac transciption factors Gata5, Hand2 and Tbx5a, the disruption of which were previously linked to impaired migration of the cardiac primordia to the embryonic midline, reduced number of myocardial precursors and failure of heart looping, respectively (Reiter et al. 1999; Yelon et al. 2000; Garrity et al. 2002). RNA-seq was performed from homozygous gata5tm236a/tm236a, tbx5am21/ m21, hand2s6/s6 mutant 72 hpf embryos in Tg(myl7:EGFP) genetic background. Homozygous mutant embryos for analyses were selected on the basis of their phenotypes of cardia bifida (gata5tm236a/tm236a, hand2s6/s6) or heart-string (tbx5am21/ m21) .
2019-01-10 | GSE120236 | GEO
Project description:The ribosome is a translational apparatus that comprises about 80 ribosomal proteins and four rRNAs. Recent studies reported that ubiquitination of the ribosomal proteins plays a pivotal role in translational control and ribosome-associated quality control (RQC). However, little is known about the dynamics of ribosome ubiquitination under complex biological processes of multicellular organisms. To study ribosome ubiquitination during animal development, we generated a zebrafish strain that expresses a FLAG-tagged ribosomal protein Rpl36/eL36 from its endogenous locus. Combining affinity purification of ribosomes from rpl36-FLAG zebrafish embryos with immunoblotting analysis, we analyzed ribosome ubiquitination during zebrafish development. Our data showed that ubiquitination of ribosomal proteins dynamically changed as development proceeded. We further revealed that Znf598, an E3 ubiquitin ligase that triggers RQC, contributed to the ribosome ubiquitination during zebrafish development. LC-MS/MS analysis and immunoblotting analysis identified lysines 139 of ribosomal protein Rps10/eS10 as pivotal ubiquitination sites on the ribosome during development. Finally, we demonstrated that an Rps10 K139/140R mutation reduced overall ribosome ubiquitination pattern. Collectively, these results reveal dynamics and complexity of ribosome ubiquitination in zebrafish development.
2023-10-11 | PXD039560 | JPOST Repository
Project description:Unlike the adult mammalian heart, which has limited regenerative capacity, the zebrafish heart can fully regenerate following injury. Reactivation of cardiac developmental programmes is considered key to successfully regenerating the heart, yet the regulatory elements underlying the response triggered upon injury and during development remain elusive. Organ-wide activation of the epicardium is essential for zebrafish heart regeneration and is considered a potential regenerative source to target in the mammalian heart. Here we compared the transcriptome and epigenome of the developing and regenerating zebrafish epicardium by integrating gene expression profiles with open chromatin ATAC-seq data. We identified epicardial enhancer elements with specific activity during development or during adult heart regeneration. By generating gene regulatory networks associated with epicardial development and regeneration, we inferred genetic programmes driving each of these processes, which were largely distinct. We identified Wt1a, Wt1b, and the AP-1 subunits Junbb, Fosab and Fosb as central regulators of the developing network, whereas Hif1ab, Nrf1, Tbx2b and Zbtb7a featured as putative central regulators of the regenerating epicardial network. Targeting hif1ab, nrf1, tbx2b and zbtb7a using CRISPR/Cas9 in injured hearts resulted in elevated epicardial cell numbers infiltrating the wound and excess fibrosis after cryoinjury, illustrating the functional importance of these regulatory factors during zebrafish heart regeneration. Our work reveals striking differences between the regulatory blueprint deployed during epicardial development and regeneration. These findings underline that heart regeneration goes beyond the reactivation of developmental programmes and provide important insights into epicardial regulation.
2023-12-01 | GSE178751 | GEO
Project description:By using transgenic zebrafish lines Tg(nxk2.5:GFP) (Witzel et al. 2012) and Tg(myl7:EGFP) (D'Amico et al. 2007), we have characterized chromatin accessibility of FACS-isolated CM (GFP+) from developing zebrafish heart at 24, 48 and 72 hpf, corresponding to heart tube formation, chamber formation and differentiation and heart maturation, respectively. GFP- cells were used as a control. We have identified cardiac regulatory networks playing a crucial role in heart morphogenesis. To validate their importance in heart development, we employed zebrafish mutants of cardiac transciption factors Gata5, Hand2 and Tbx5a, the disruption of which were previously linked to impaired migration of the cardiac primordia to the embryonic midline, reduced number of myocardial precursors and failure of heart looping, respectively (Reiter et al. 1999; Yelon et al. 2000; Garrity et al. 2002). ATAC-seq was performed from homozygous gata5tm236a/tm236a, tbx5am21/ m21, hand2s6/s6 mutant 72 hpf embryos in Tg(myl7:EGFP) genetic background. Homozygous mutant embryos for analyses were selected on the basis of their phenotypes of cardia bifida (gata5tm236a/tm236a, hand2s6/s6) or heart-string (tbx5am21/ m21) .
2019-01-10 | GSE120237 | GEO
Project description:Tbx5 paralogues during zebrafish development
| PRJNA475603 | ENA
Project description:Adult zebrafish, in contrast to mammals, are able to regenerate their hearts in response to injury or experimental amputation. Our understanding of the cellular and molecular bases that underlie this process, although fragmentary, has increased significantly over the last years. However, the role of the extracellular matrix (ECM) during zebrafish heart regeneration has been comparatively rarely explored. Here, we set out to characterize the ECM protein composition in adult zebrafish hearts, and whether it changed during the regenerative response. For this purpose, we first established a decellularization protocol of adult zebrafish ventricles that significantly enriched the yield of ECM proteins. We then performed proteomic analyses of decellularized control hearts and at different times of regeneration. Our results show a dynamic change in ECM protein composition, most evident at the earliest (7 days post-amputation) time-point analyzed. Regeneration associated with sharp increases in specific ECM proteins, and with an overall decrease in collagens and cytoskeletal proteins. We finally tested by atomic force microscopy that the changes in ECM composition translated to decreased ECM stiffness. Our cumulative results identify changes in the protein composition and mechanical properties of the zebrafish heart ECM during regeneration.
2019-08-26 | PXD010092 | Pride
Project description:Ischemic cardiopathy is the leading cause of death in the world, for which efficient regenerative therapy is not currently available. In mammals, after a myocardial infarction episode, the damaged myocardium is replaced by scar tissue featuring collagen deposition and tissue remodelling with negligible cardiomyocyte proliferation. Zebrafish, in contrast, display an extensive regenerative capacity as they are able to restore completely lost cardiac tissue after partial ventricular amputation. Due to the lack of genetic lineage tracing evidence, it is not yet clear if new cardiomyocytes arise from existing contractile cells or from an uncharacterised set of progenitors cells. Nonetheless, several genes and molecules have been shown to participate in this process, some of them being cardiomyocyte mitogens in vitro. Though questions as what are the early signals that drive the regenerative response and what is the relative role of each cardiac cell in this process still need to be answered, the zebrafish is emerging as a very valuable tool to understand heart regeneration and devise strategies that may be of potential value to treat human cardiac disease. Here, we performed a genome-wide transcriptome profile analysis focusing on the early time points of zebrafish heart regeneration and compared our results with those of previously published data. Our analyses confirmed the differential expression of several transcripts, and identified additional genes the expression of which is differentially regulated during zebrafish heart regeneration. We validated the microarray data by conventional and/or quantitative RT-PCR. For a subset of these genes, their expression pattern was analyzed by in situ hybridization and shown to be upregulated in the regenerating area of the heart. The specific role of these new transcripts during zebrafish heart regeneration was further investigated ex vivo using primary cultures of zebrafish cardiomyocytes and/or epicardial cells. Our results offer new insights into the biology of heart regeneration in the zebrafish and, together with future experiments in mammals, may be of potential interest for clinical applications. In order to study zebrafish heart regeneration, a time course experiment was realized where amputated heart regenerating were compared to control heart. Samples in triplicate were extracted at 1, 3, 5 and 7 days post-amputation.
2010-03-09 | E-GEOD-17993 | biostudies-arrayexpress