Mitochondrial fission and fusion dynamics are critical cellular processes, and abnormalities in these processes are associated with severe human disorders, such as Beckwith-Wiedemann syndrome, neurodegenerative diseases, Charcot-Marie-Tooth disease type 6, multiple symmetric lipomatosis and microcephaly. Fuzzy onions protein 1 (Fzo1p) regulates mitochondrial outer membrane fusion. In the present study, Schizosaccharomyces pombe ( S. pombe ) was used to explore the effect of FZO1 gene deletion on cell dynamics in mitosis. The mitochondrial morphology results showed that the mitochondria appeared to be fragmented and tubular in wild-type cells; however, they were observed to accumulate in fzo1Δ cells. The FZO1 gene deletion was demonstrated to result in slow proliferation, sporogenesis defects, increased microtubule (MT) number and actin contraction defects in S. pombe . The FZO1 gene deletion also affected the rate of spindle elongation and phase time at the metaphase and anaphase, as well as spindle MT organization. Live-cell imaging was performed on mutant strains to observe three distinct kinetochore behaviors (normal, lagging and mis-segregation), as well as abnormal spindle breakage. The FZO1 gene deletion resulted in coenzyme and intermediate metabolite abnormalities as determined via metabolomics analysis. It was concluded that the loss of FZO1 gene resulted in deficiencies in mitochondrial dynamics, which may result in deficiencies in spindle maintenance, chromosome segregation, spindle breakage, actin contraction, and coenzyme and intermediate metabolite levels.

Mitochondria are dynamic organelles that undergo cycles of fission and fusion. The major mitochondrial fission protein is dynamin-related Drp1 GTPase (Dnm1 in yeast). The effects of Dnm1 gene deletion on cell dynamics and energy metabolism during mitosis were studied in Schizosaccharomyces pombe. Dnm1 gene deletion can lead to slow growth, abnormal sporulation, abnormal number and length of interphase microtubules of Schizosaccharomyces pombe. The deletion of Dnm1 gene can also affect the spindle growth speed and growth time of metaphase and anaphase, and affect the spindle fluorescence intensity of prophase and metaphase. At the same time, the structure and dynamics of the spindle microtubules of Dnm1Δ are also different. The statistics of spindle length showed that there was delayed spindle fracture in Dnm1Δ Cells. Two different chromosome behaviors, normal and lagged, were observed by living cell imaging. The analysis of coenzymes, intermediates and energy in energy metabolism showed that there were some abnormalities after Dnm1 gene deletion, including coenzyme defects, intermediate metabolite defects and ATP production defects.