Open Access

Filomena Ricciardi

• In conclusion our data show, that Flightless I function is essential for striated muscle development in zebrafish. Myofibrillar bundling and focal adhesion formation represent the basis for this development, and are ultimately a prerequisite for cardiac trabeculation. Future analysis of Actin polymerization in trabeculation will provide addition knowledge about the sensitivity of the developing and adult heart to a disequilibrium in F-actin versus G-actin availability. In this study we found a novel ErbB2-dependent cardiomyocyte maturation process which affects both cardiac chambers. It will be of great interest to further study the nature of the Memo1-GFP cell-cell junctions and other junction proteins in order to unravel the significance of this maturation process for heart development. Interestingly we found, that memo1bns4 homozygous mutant animals, which we generated with CRISPR/Cas9 technology, develop indistinguishable from siblings, suggesting that zygotic memo1 expression is dispensable for zebrafish development. Future studies will address the question if maternal zygotic memo1bns4 mutants will develop a heart or vascular phenotype as reported form Memo1 knockout mice or as observed in memo1 morphants in this study. In cultured C2 mouse skeletal muscle cells the Golgi-apparatus relocalizes dependent on centrosomal proteins and independent of microtubules. We describe here that zebrafish cardiomyocytes have a similar Golgi-complex distribution suggesting a similar differentiation-dependent reorganization. This striated muscle specific, fragmented Golgi distribution might be an advantage for these cells in order to shuttle vesicles through the densely packed sarcomere structures. Future studies could address the timing of the Golgi-reorganization in cardiomyocytes during development and possibly use this Golgi-zebrafish line as a tool to study cardiomyocyte maturation in disease models and in heart regeneration.