Quaking are RNA binding proteins, which are known to regulate the expression of different genes at the post-transcriptional level. Genetic interference with quaking a (qkia) and quaking c (qkic) leads to major myofibril defects during zebrafish development, without affecting early muscle differentiation. In order to understand how qkia and qkic jointly regulate myofibril formation, we performed a comparative analysis of the transcriptome of qkia/qkic (qkia mutant injected with qkic morpholino) versus control embryos. We show that Quaking activity is required for accumulation of the muscle-specific tropomyosin 3 transcript, tpm3.1. Whereas interference with tmp3.1 function disrupts myofibril formation, reintroducing tpm3.1 transcripts into embryos with reduced Quaking activity can restore structured myofibrils. Thus, we identify tropomyosin as an essential component in the process of myofibril formation and as a relay downstream of the regulator proteins Quaking. Overall design: Transcriptome of control versus qkia/qkic embryos at 24-26hpf. Biological triplicate were prepared for both condition (3x2 samples).
Quaking RNA-Binding Proteins Control Early Myofibril Formation by Modulating Tropomyosin.
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View Sampleswt1a:GFP labels a population of subepicardial cells in the uninjured ventricle. Here we compare the expression profile of wt1a:GFP-positive cells to the rest of the cells of the ventricle. Overall design: Four paired biological replicates of wt1a:GFP-positive and wt1a:GFP-negative cells obtained from pools of 3-5 zebrafish heart ventricles.
Transient fibrosis resolves via fibroblast inactivation in the regenerating zebrafish heart.
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