Mitochondria are maternally inherited in many organisms. Mitochondrial morphology and activity regulation is essential for cell survival, differentiation and migration. An analysis of mitochondrial dynamics and function in morphogenetic events in early metazoan embryogenesis has not been carried out. In our study we find a crucial role of mitochondrial morphology regulation in cell formation in Drosophila embryogenesis. We find that mitochondria are small, fragmented and translocate apically on microtubules and distribute progressively along the cell length during cellularization. Embryos mutant for mitochondrial fission protein, Drp1, die in embryogenesis and show an accumulation of clustered mitochondria on the basal side in cellularization. Additionally, Drp1 mutant embryos contain lower levels of reactive oxygen species (ROS). ROS depletion has been previously shown to decrease Myosin II activity. Drp1 loss also leads to Myosin II depletion at the membrane furrow thereby resulting in decreased cell height and larger contractile ring area in cellularization similar to Myosin II mutants. The mitochondrial morphology and cellularization defects in Drp1 mutants are suppressed by reducing mitochondrial fusion and increasing cytoplasmic ROS in superoxide dismutase mutants. Our data show a key role for mitochondrial morphology and activity in supporting the morphogenetic events that drive cellularization in Drosophila embryos.

线粒体是许多生物的母系遗传。线粒体形态和活性调节对于细胞存活，分化和迁移至关重要。尚未进行早期子生后胚胎发生中线粒体动力学和形态发生事件中的功能的分析。在我们的研究中，我们发现果蝇中线粒体形态调控在细胞形成中的关键作用胚胎发生。我们发现线粒体很小，碎片化，在微管上顶端移位，并在细胞化过程中沿细胞长度逐渐分布。线粒体分裂蛋白Drp1的胚胎突变体在胚胎发生中死亡，并在细胞化过程中在基底侧显示成簇的线粒体积累。此外，Drp1突变体胚胎包含较低水平的活性氧（ROS）。先前已证明ROS消耗会降低肌球蛋白II活性。Drp1丢失还导致膜沟处的肌球蛋白II耗竭，从而导致细胞高度降低，并且在细胞化过程中类似于肌球蛋白II突变体产生更大的收缩环面积。通过减少线粒体融合和增加超氧化物歧化酶突变体中的细胞质ROS，可以抑制Drp1突变体中的线粒体形态和细胞化缺陷。我们的数据显示线粒体形态和活性在支持驱动细胞凋亡的形态发生事件中起着关键作用。果蝇胚胎。