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Fig. 1 Acquisition and phenotypic analysis of tnnt2a−/− zebrafish. A Model 1 is the tnnt2a−/− homozygous juveniles produced by self-crossing of tnnt2a heterozygotes. Nevertheless, the homozygous mutant model used in this study has only a 25% probability of being obtained through self-crossing, and it exhibits a high mortality rate. To address these limitations, we employed the Tg:Tnnt2a−/− transgenic zebrafish model (referred to as Model 2) in our study. This model features a recovered heartbeat after the addition of DOX, allowing for more reliable and sustainable experimental conditions. B Representative images of lateral view of AB and tnnt2a−/− zebrafish. At 2 dpf, the tnnt2aex10Δ2 ( tnnt2a−/−) exhibits a phenotype reminiscent of dilated cardiomyopathy, characterized by cardiac arrest and enlargement of both the atrium and ventricle. Concurrently, mutant zebrafish display significant pericardial effusion, a hallmark of heart failure, at approximately 3 dpf