During heart formation, the heart grows and undergoes dramatic morphogenesis to achieve efficient embryonic function. Both in fish and amniotes, much of the growth occurring after initial heart tube formation arises from second heart field (SHF)-derived progenitor cell addition to the arterial pole, allowing chamber formation. In zebrafish, this process has been extensively studied during embryonic life, but it is unclear how larval cardiac growth occurs beyond 3 days post-fertilisation (dpf). By quantifying zebrafish myocardial growth using live imaging of GFP-labelled myocardium we show that the heart grows extensively between 3 and 5 dpf. Using methods to assess cell division, cellular development timing assay and Kaede photoconversion, we demonstrate that proliferation, CM addition, and hypertrophy contribute to ventricle growth. Mechanistically, we show that reduction in Mef2c activity (mef2ca^+/−;mef2cb^−/−), downstream or in parallel with Nkx2.5 and upstream of Ltbp3, prevents some CM addition and differentiation, resulting in a significantly smaller ventricle by 3 dpf. After 3 dpf, however, CM addition in mef2ca^+/−;mef2cb^−/− mutants recovers to a normal pace, and the heart size gap between mutants and their siblings diminishes into adulthood. Thus, as in mice, there is an early time window when SHF contribution to the myocardium is particularly sensitive to loss of Mef2c activity.

在心脏形成过程中，心脏生长并经历剧烈的形态发生，以实现有效的胚胎功能。在鱼类和羊膜动物中，最初的心管形成后发生的大部分生长都来自于第二心脏场（SHF）衍生的祖细胞添加到动脉极，从而形成了小室。在斑马鱼中，已经在胚胎生命中对此过程进行了广泛的研究，但尚不清楚受精后（dpf）超过3天后幼虫心脏的生长如何发生。通过使用GFP标记的心肌的实时成像定量斑马鱼的心肌生长，我们显示出心脏在3 dpf和5 dpf之间广泛生长。使用评估细胞分裂的方法，细胞发育时间测定和Kaede光转换，我们证明增殖，CM添加和肥大有助于心室的生长。mef2ca ^+/- ; mef2cb ^-/-），在Nkx2.5的下游或与之并行，在Ltbp3的上游，阻止了某些CM的添加和分化，导致心室明显缩小了3 dpf。然而，在3 dpf后，mef2ca ^+/- ; mef2cb ^-/-突变体中的CM添加恢复正常，并且突变体及其同胞之间的心脏大小差距逐渐减小，直至成年。因此，就像在小鼠中一样，当SHF对心肌的贡献对Mef2c活性的丧失特别敏感时，存在一个早期的时间窗口。