SRA

Mitochondrial energy production is essential for development, yet the mechanisms underlying the continuous increase in mitochondrial activity during embryogenesis remain elusive. Using zebrafish as a model system for vertebrate development, we identify two sequentially acting mechanisms that could contribute to the rise in mitochondrial activity: an increased association between mitochondria and the endoplasmic reticulum (ER) at early stages, followed by the fusion of mitochondria leading to their elongated morphology at later embryonic stages. By comprehensively profiling mitochondrial activity, abundance, morphology, metabolome, proteome and phospho-proteome as well as respiratory chain enzymatic activity, we find that the increase in mitochondrial activity during embryogenesis does not require mitochondrial biogenesis, is not limited by metabolic substrates at early stages, and occurs under steady levels of respiratory chain complexes and enzymatic activities. Instead, our analyses pinpoint a previously unexplored increase in mitochondrial-ER association during early stages in combination with changes in mitochondrial morphology at later stages as possible contributors to the rise in mitochondrial activity during embryogenesis. Overall, our systematic profiling of the molecular and morphological changes to mitochondria during embryogenesis provides a valuable resource for further studying mitochondrial function during embryogenesis. Overall design: To investigate whether oligomycin-treated embryos, we performed RNA-seq experiment to detect ZGA genes. As a control we used untreated and actinomycin-injected embryos to block zygotic transcription.