Mitochondrial fission regulates ROS for ventral furrow formation in Drosophila gastrulation

Mitochondrial fusion and fission are essential for embryogenesis, but the mechanisms by which they regulate morphogenesis are not entirely understood. In this study, we elucidate the role of mitochondrial fission in Drosophila gastrulation. We find that fragmented mitochondria migrate apically in constricting ventral cells in a microtubule and Dorsal/NFkb dependent manner. Reduced mitochondrial fission in Drp1 mutant embryos leads to accumulation of larger mitochondria basally and fewer apical mitochondria. Drp1 mutants show decreased Myosin II, resulting in defective ventral furrow formation. Transcriptomic analysis from Drp1 mutants shows no changes in the Dorsal signaling pathway. Proteomic analysis reveals increased levels of antioxidant enzymes and decreased respiratory complexes, resulting in low ROS levels. Depleting SOD2 in Drp1 mutants restores ROS levels, allowing apical mitochondrial migration, Myosin II increase and proper ventral furrow formation. Our study reveals a significant role for mitochondrial dynamics and activity for apical constriction during gastrulation.