UNASSIGNED: During the cell cycle, mitochondria undergo regulated changes in morphology. Two particularly interesting events are first, mitochondrial hyperfusion during the G1-S transition and second, fragmentation during entry into mitosis. The mitochondria remain fragmented between late G2- and mitotic exit. This mitotic @entity2383 constitutes a checkpoint in some cell types, of which little is known. We bypass the 'mitotic @entity2383 ' checkpoint by inducing fragmented mitochondrial morphology and then measure the effect on cell cycle progression. Using @entity238 larval hemocytes, @entity238 S2R+ cell and cells in the pouch region of wing imaginal disc of @entity238 larvae we show that inhibiting mitochondrial fusion, thereby increasing fragmentation, causes cellular hyperproliferation and an increase in mitotic index. However, @entity2383 due to over-expression of the mitochondrial fission machinery does not cause these changes. Our experiments suggest that the inhibition of mitochondrial fusion increases superoxide radical content and leads to the upregulation of @entity25500 that culminates in the observed changes in the cell cycle. We provide evidence for the importance of mitochondrial superoxide in this process. Our results provide an insight into the need for @entity38986 -degradation during mitosis and also help in understanding the mechanism by which mitofusins may function as @entity5 suppressors.

XXXX Due to Inhibition of Fusion Increases @entity25500 through Mitochondrial Superoxide Radicals.

@entity38986 :: ('31581(Tax:7227)', 'Gene') :: ['mitofusin'] @entity5 :: ('MESH:D009369', 'Disease') :: ['tumor'] @entity25500 :: ('37618(Tax:7227)', 'Gene') :: ['cyclin B'] @entity238 :: ('7227', 'Species') :: ['Drosophila'] @entity2383 :: ('MESH:D028361', 'Disease') :: ['mitochondrial fragmentation']
@entity2383 :: (MESH:D028361,Disease) :: ['Mitochondrial Fragmentation']
